The two main compartments of ECF

BODY FLUID AND ELECTROLYTES are:

 Gender
In good health, a delicate balance of 1. Intravascular
MALE – 60%
fluids, electrolytes, acids, and bases Intravascular fluid, or plasma,
 There is a greater
maintains the body. accounts for approximately 1/3 of ECF
amount of water in the
This balance, or homeostasis, and is found within the vascular
male body than in the
depends on multiple physiological system.2. Interstitial
female body.
processes that regulate fluid intake 2. Interstitial fluid, accounting for
 Males are more muscular
and output, as well as the approximately 2/3 of ECF,
than females.
movement of water and the surrounds the cells. (3rd space
 Muscles can store water.
substances dissolved in it between edema)
FEMALE – 50%
Computation for ECF:
body compartments.  Females have more
Almost every illness has the Ex. 70 kgs., Male=60% ECF=
adipose tissue than
potential to threaten this balance. 33%
males.
70 kgs. x 0.6 = 42kg
Even in daily living, factors such as  Fats do not store water.
excessive temperatures or vigorous = 42L
activity can disturb homeostasis if = 42 x .33
Distribution of Body Fluids
adequate water and salt intake are = 13.86
The body's fluid is divided into two
not maintained. Plasma 13.86 ÷ 1/3 = 4.62
major compartments:
Therapeutic measures, such as the  Intracellular fluid (ICF)
use of diuretics or nasogastric  Found within the cells of
suction, can also disturb the body's the body.
homeostasis unless water and  Constitutes
electrolytes are replaced. approximately two-thirds
Water is vital to health and normal of the total body fluid in
cellular function, serving as: adults. (2/3 or 67%)
1. A medium for metabolic  Vital to normal cell
reactions within cells. functioning. It contains
2. A transporter for nutrients, solutes such as oxygen,
waste products, and other electrolytes, and glucose,
 The other compartments of ECF
substances or PLASMA. andthe
it provides a medium
include lymph and
3. A lubricant (Peritoneal cavity/ in whichfluids.
the metabolic
transcellular
Pericardial cavity). processes of the cell
Examples of transcellular fluidtake
4. An insulator and shock place.
include:
absorber (joints). Computation  for ICF:
cerebrospinal.
5. A means of regulating and Ex. 70 kgs., Male=60%, ICF=67%
pericardial.
maintaining body 70 kgs. x 0.6= 42kg
 pancreatic,
temperature (fever). = 42L x .67
 pleural,
6. Eliminate waste Products = 28.14L
 intraocular,
(kidneys).
 biliary,
 50-60% of body weight is  Extracellular fluid (ECF)
 peritoneal, and
water.  Found outside the cells.
synovial fluids
Two factors that influence body  Accounts for about one-
water distribution: third of total body fluid.
 Age (1/3 or 33%)
INFANT – 70%-80%  Although ECF is
 Fluids in the ECF can the smaller of the two
easily be lost. compartments, it is the
 The fluid-electrolyte transport system that
balance of an infant carries oxygen and
can easily be upset. nutrients to, and waste
products from, body
cells.
SYSTEMIC ROUTES OF GAINS AND
LOSSES
 Systemic Routes of Gains and
Losses Water and electrolytes
are gained in various ways.
 Healthy people gain fluids by
drinking and eating, and their
daily average intake and output
(I & O) of water are
approximately equal (Table 10-
2).

INSENSIBLE WATER LOSS

 Is invisible vaporization from
the lungs and skin. Normally,
600 to 900 ml/day is lost.
 Only water is lost by insensible
perspiration.
 Excessive sweating (sensible
perspiration) due to fever, or
high environmental Specialized neurons in the
temperature causes large hypothalamus:
losses of water and electrolytes.  Highly sensitive to serum
BODY FLUID REGULATION osmolality.
 Under normal conditions, the  Increased osmolality –
following mechanisms regulate osmoreceptors stimulate
normal fluid volume and the hypothalamus to
electrolyte concentrations: synthesize ADH
 Osmoreceptors (↓) (vasopressin).
 ADH – anti-diuretic  Decreased osmolality –
hormone (↓) ADH (vasopressin) is
 RAAS – renin angiotensin inhibited.
aldosterone system (↓) (ADH: Retains water in the renal
 ANP – anti-natriuretic tubules)
peptide (↑) Triggers thirst promoting increased
fluid intake.
 Thirsty when ECF volume
decreases by approx. 700ml
(2% of body weight).
Also sensitive to changes in BV & BP
through the info relayed by
baroreceptors (stretch).  Capillary forces are the two
forces at every capillary
Fluids & electrolytes move among membrane:
cells, compartments, tissue spaces,  Hydrostatic pressure (also
and plasma by the processes of: called hydraulic pressure) - is
 Osmosis the pressure exerted by fluid on
- Movement of the walls of the blood vessel.
water/liquid/solvent o Hydrostatic pressure
across a semi-permeable pushes fluid out of the
membrane from a lesser capillary toward the ICF.
concentration to a higher  Osmotic pressure - is the
concentration. pressure exerted by the solutes
Osmolality and osmolarity within the plasma.
are terms that describe the o Osmotic pressure pulls
concentration of solutes or fluid into the capillary
dissolved particles in a from the ICF.
solution. These forces oppose each other at
- every capillary membrane and
 Diffusion balance each other out in healthy
 Filtration and (homeostatic) conditions.
 Active transport
OSMOSIS
 Movement of
water/liquid/solvent across a
semi-permeable membrane
from a lesser concentration to a
higher concentration.
Osmolality and osmolarity are terms
that describe the concentration of
solutes or dissolved particles in a
solution.
 Osmolality - is the number of
milliosmoles of solute (the
standard unit of osmotic
pressure) per kilogram of ONCOTIC PRESSURE
solvent; it is expressed as  Osmotic pressure specifically
milliosmoles per kilogram exerted by the albumin within
(mOsm/kg). the bloodstream is termed
 Osmolarity - is the number of colloid oncotic pressure or
milliosmoles (the standard unit colloid osmotic pressure.
of osmotic pressure) per liter of  A colloid is a fluid consisting of
solution; it is expressed as non-soluble substances that are
milliosmoles per liter (mOsm/L). evenly distributed within a
solvent. Blood is an example of
a colloid solution. It is a mixture
of blood cells and plasma which
contains water, proteins,
enzymes, and other solutes.
DIFFUSION
 Movement of particles, solutes,
and molecules from an area of
higher concentration to an area
of a lower concentration
Regulation of Fluid within the Body through a semi-permeable
Compartments membrane.
 Normal movement of fluids  Factors affecting the rate of
through the capillary wall into diffusion:
the tissues depends on a. Size of the molecules: larger
Starling’s Laws of Capillary size moves slower than smaller
Forces. size.
 b. Concentration of solution: wide concentration to higher
difference in concentration has concentration using energy
a faster rate of diffusion. (ATP)
c. Temperature: ↑ in T = ↑ rate of  e.g., Na-K pump
diffusion SODIUM-POTASSIUM PUMP

FACILITATED DIFFUSION
 Require assistance from a
carrier molecule to pass
through a semi-permeable
membrane.
 E.g., insulin-glucose.
COMPOSITION OF BODY FLUID
Extracellular and intracellular fluids
contain oxygen from the lungs,
dissolved nutrients from the
gastrointestinal tract, excretory
products of metabolism such as
carbon dioxide, and charged particles
called “ions”.
ELECTROLYTES
Substances present in ICF & ECF carry
an electrical charge. These charged
particles are called electrolytes.
 Cations (+)
FILTRATION o The major “cations” in
 Movement of both solute and body fluid are sodium,
solvent across a semi- potassium, calcium,
permeable membrane from an magnesium, and
area of higher pressure to lower hydrogen ions.
pressure  Anions (-)
 Movement of water and solutes o The major “anions” are
occurs from an area of high chloride, bicarbonate,
hydrostatic pressure to an area phosphate, sulfate, and
of low hydrostatic pressure. negatively charged
 Example: The kidneys filter protein ions.
approximately 180 L of plasma
per day.

ACTIVE TRANSPORT
 Movement of solute from lower
 activities (a decrease of 1
meq/L = 25% difference in total
ECF K+ concentration)
POTASSIUM (K+) Regulator
 Aldosterone and hydrogen ions
regulate potassium levels.
 Aldosterone retains sodium and
excretes potassium.
FUNCTION OF ELECTROLYTES IN THE  (Aldosterone is pro-Na+,”
BODY and anti – K+.”)
1. Promote neuromuscular  Increase aldosterone
irritability (muscle contraction secretion: Hypokalemia
and relaxation).  Decrease aldosterone
2. Maintain body fluid volume and secretion:
osmolality. Hyperkalemia
3. Distribute body water between  Alkalosis increases potassium
fluid compartments. excretion resulting in
4. Regulate acid-base balance. Hypokalemia.
 Acidosis decreases potassium
SODIUM (Na+) excretion resulting in
135-145mEq/L (mmol/L) Hyperkalemia.
 Major cation in ECF; major (Alkalosis: Hypokalemia; Acidosis:
contributor of plasma Hyperkalemia)
osmolality
 ECF Na+ level determines CALCIUM (Ca++)
whether water is retained, 8.8-10.5 mg/dl (2.25-2.75 mmol/L)
excreted, or translocated.  2 forms: bound & unbound
 Functions: (ionized)
Skeletal/ heart muscle contraction, Bound: attached to CHON (albumin)
nerve impulse transmission, Normal Unbounded (Ionized): “free” calcium;
ECF osmolality, Normal ECF volume. active form; ECF
SODIUM (Na+) and Water Regulator  Functions:
 Thirst: The major control of Bone strength & density, activation of
actual fluid intake. The thirst enzymes or reactions, skeletal/
center in the hypothalamus is cardiac muscle contraction, nerve
activated once the body loses impulse transmission, and blood
at least 2% of fluids. clotting.
 Kidneys: The major organs CALCIUM(Ca++) Regulation
controlling output.  Ca++ and phosphorus: 99%
excrete an average of 1,500 ml found in bones and teeth, 1% in
of fluids/day in the form of urine. blood.
 ADH. Retain water in the renal  Ca++ and phosphorus have
tubules. an inverse relationship.
 RAAS. Aldosterone retains  If both are elevated:
sodium and water. an insoluble precipitate will
Sodium primarily determines form.
the osmolality (concentration) of body  Low total CHON(Protein) and
fluids. albumin: low total serum Ca++
 Parathormone (PTH) elevates
POTASSIUM (K+) serum calcium levels through
(ECF: 3.5-5.0mEq/L or mmol/L) the withdrawal of calcium from
 Major ICF cation bones or bone resorption.
 Functions: Regulates CHON  Increase PTH: Increase
synthesis, glucose use & serum calcium
storage, maintains action  Decrease PTH: Decrease
potentials in excitable serum calcium
membranes  Thyrocalcitonin lowers serum
 Any change in blood K+ calcium levels by depositing
seriously affects physiological calcium into the bone.
 Increase Thyrocalcitonin:
 decrease serum calcium 290 mOsm/L
 Decrease  ISOTONIC fluid: Body fluids are
Thyrocalcitonin: Increase ISOTONIC comparable with
serum calcium 0.9% NaCl
 Vitamin D promotes calcium  HYPOTONIC fluids have a
absorption. lesser or lower solute conc.
than plasma; ex. is 0.45%,
PHOSPHORUS (P) 0.33%NaCl solution
2.5-4.5 mg/dl (0.8-1.45 mmol/L)  HYPERTONIC fluids have a
 Major anion ICF (80% is in higher or greater conc. of
bones) solutes (usually sodium)
 Functions: compared with plasma; ex. is
 Activating B-complex vitamins, D5 NS
ATP, assisting in cell division,
cooperating in CHO, CHON &
FAT metabolism, acid-base
buffering, calcium homeostasis;
balanced & reciprocal
relationship w/ Ca++
PHOSPHORUS (P) Regulator
 Regulated by PTH: ↑ PTH = ↓
P
↓ PTH = ↑
P
MAGNESIUM (Mg++)
1.8-3.6 mg/dl (0.75-1.07 mmol/L)
 60% stored in bones &
cartilage; much more is stored
in ICF (heart, liver, skeletal
muscles)
 Functions:
 ICF – skeletal muscle
contractions, CHO
metabolism, ATP
formation, Vitamin B-
complex activation, DNA
synthesis, CHON
synthesis
 ECF – regulates blood
coagulation & skeletal
muscle contractility
 Regulated by the kidney & GIT
(exact mechanisms are not
known)

CHLORIDE (Cl-)
98-106 meq/L (mmol/L)
 Major ECF anion; work with Na+
to maintain ECF osmotic
pressure
 Important in the formation of
HCL in the stomach
 Participates in chloride shift
(exchange between Cl- & HCO3-)

TONICITY OF BODY FLUIDS

 Refers to the concentration of
particles in a solution
 The normal tonicity or
osmolarity of body fluids is 275-
 o Lack of access to fluids
o Third – space fluid shifts
 Edema (In burn) – interstitial
space
 Ascites (liver dysfunction) –
peritoneal cavity
 Diabetes insipidus – dry inside
↓ADH
 Decreased ability to
concentrate urine (deficit of
ADH or nephron resistance to
ADH)
 Interferes with water
reabsorption
 Adrenal insufficiency
 Impaired production of
aldosterone
 Adrenal insufficiency
 Osmotic diuresis
 increase in urine output
 Hemorrhage (bleeding) – FV
loss
 Coma
CLINICAL MANIFESTATIONS:
FLUID VOLUME IMBALANCES
 Acute weight loss
FLUID VOLUME DISTURBANCES  ↓ skin turgor – pinch skin
Hypovolemia ↓ blood volume  Oliguria
 Fluid volume deficit (FVD), or  Concentrated urine - tea-
hypovolemia, occurs when loss colored urine
of ECF volume exceeds the  Capillary filling time prolonged
intake of fluid. (3 seconds)
 It occurs when water and  ↓ CVP
electrolytes are lost in the same  ↓ BP
proportion as they exist in  Flattened neck veins – jugular
normal body fluids, so that the veins
ratio of serum electrolytes to  Dizziness
water remains the same.  Weakness
 Serum electrolyte  Thirst and confusion
concentrations can remain  ↑ pulse
normal, increase, or increase in  Muscle cramps – anaerobic
FVD. metabolism and lactic acidosis
Different from dehydration  Sunken eyes
 FVD (hypovolemia) should not  Nausea
be confused with  ↑ temperature - ↓ body fluid
DEHYDRATION, which refers to  Cool, clammy, pale skin - shock
loss of water alone, with DIAGNOSTICS:
increased serum sodium levels.  ↑ Hgb and Hct – concentrated
 FVD may occur alone or in blood cells
combination with other  ↑ Serum osmolality –
imbalances. concentrated body fluids
CAUSES:  ↑ Urine osmolality
 Loss of body fluids + ↓ fluid  ↑ Urine specific gravity
intake  ↓ Urine Na
 Abnormal fluid losses  ↑ BUN and Creatinine – poor
o Vomiting kidney function
o Diarrhea GERONTOLOGICAL CONSIDERATIONS:
o GI suctioning  I & O from all sources
o Sweating o Same type of clothing
o Decreased intake o Same weighing scale
o Nausea
 o Same time – proper fluid replacement.
endorsement o Administer 100 to 200
 Daily weight – to monitor for mL of normal saline
gain or loss solution over 15 minutes
 Side effect & interaction of  Vital signs
medications  Breath sounds (crackles if fluid
 Documentation and prompt is not processed by kidneys.)
reporting of disturbances  Sensorium
 In most adult patients, it is  CVP
useful to monitor skin turgor to  UO
detect subtle changes. o Provide fluids rapidly
 Not as valid in older adults enough to attain
because the skin has lost adequate tissue
elasticity. perfusion without
 Slowness in the filling of veins compromising the
of the hands and feet (also cardiovascular system.
check for capillary refill and  ↑ UO, ↑ BP (from ↓BP), ↑ CVP
tongue appearance if small & (Normal renal function)
with longitudinal fissures)  Shock (Hypovolemic) – usually
 Functional assessment caused by bleeding)
 The nurse provides if the - 25% intravascular
patient is unable to carry out volume loss or rapid fluid
self-care activities volume loss.
 ↓ oral fluid intake due to
avoidance of urinary
Incontinence
 Wear diapers
 Urinal (bedside commode)
 Pace fluid intake
 Remind to drink adequate fluids
(very warm or humid weather)
MEDICAL MANAGEMENT:
 Strict Monitoring (to avoid
volume overload)
o I&O
o Weight
o Vital signs
o CVP ↓Cardiac Output - ↓BP & tachycardia
o LOC
o Breath sounds
(crackles/rales = Decreased Tissue Perfusion –
pulmonary edema) tachypnea, ↓BV, cold clammy skin,
o Skin color (pale) hypoxemia, anoxia of heart, brain, &
o Treatment is based on kidney(oliguria)
the severity of fluid loss
and pt. response NURSING MANAGEMENT:
 Depressed Renal Function Intake and Output
(Oliguria)  q8, q4 or q1 in ICU (Accurate)
o Determine the cause of  May impact the mortality of
depressed renal function patients -early detection (+)(-)
 Prerenal azotemia (FVD) -  Expect a concentrated urine
↑Creatinine ↑BUN  Daily body weight
 Intrarenal azotemia (Acute  0.5 kg weight loss is
tubular necrosis from prolonged approximately 500 ml fluid loss
FVD) – AKI (acute kidney injury) Closely monitored (Hypovolemic
 fluid challenge test (While Shock)
the hemodynamic response to  Tachycardia (weak)
this treatment is monitored) –  Severe hypotension
VS & renal function while giving  Tachypnea
  ↓ peripheral pulses proportions in which they
 ↓ temperature normally exist in the ECF.
 ↓ CVP  Isotonic expansion of the ECF
 Skin and tongue turgor  ↑ in total body water (Due to ↑
 Pinch skin sodium)
 Dependent on interstitial CAUSES:
fluid volume  Fluid overload or ↓ function of
 Skin flattens more slowly the homeostatic mechanisms
and remains elevated for responsible for regulating fluid
many seconds (Severe) balance.
o Over the sternum  Heart failure
o Dorsal surface of the  Renal failure (portal
hand hypertension, ascites)
o Inner aspects of the  Cirrhosis of the liver
thighs  Another contributing factor:
o Forehead o Consumption of
o Tongue turgor is not excessive amounts of
affected by age table/other sodium salts.
 Smaller tongue o Excessive administration
 Longitudinal furrows of sodium-containing
 Dry mouth fluids.
 Urine Specific Gravity  Expansion of the ECF:
> 1.020 Edema
 Healthy renal conservation of o Ambulatory (ankles)
fluid o Supine (sacrum)
 Mental Function (Severe FVD) Distended jugular veins, and
 ↓ cerebral perfusion Crackles
(Monitor GCS) CLINICAL MANIFESTATIONS:
o Mild anxiety  Tachycardia
o Confusion and agitation  Bounding pulse
o Lack of cognition, and
delirium (plucking of
linen)
o Comatose
 Acute cardiopulmonary
decompensation
 Extensive hemodynamic
monitoring
 Preventing Hypovolemia
 Identify patients at risk and
take measures to minimize fluid
losses
 Correcting Hypovolemia
 oral fluids
 oral rehydration solutions
(ORS)
 antiemetics
If oral is not effective
 Parenteral – IV (isotonic or
hypotonic)
 Enteral - NGT

Hypervolemia ↑ blood volume

 Fluid volume excess (FVE), or
hypervolemia (congestion),
refers to an expansion of the
ECF caused by the abnormal
retention of water and sodium
in approximately the same
  ↑ BP
 ↑ CVP ↑BV
 Respiration system
o Tachypnea
o Shortness of breath
(dyspnea)
o Crackles
o Cough (moist)
o Orthopnea
Signs and Symptoms
 GI system
o Acute weight gain  Dialysis
o Ascites – fluid in o Hemodialysis
peritoneal space o Peritoneal dialysis
(paracentesis)
 Other s/sx
o Peripheral edema
o Jugular vein distention
o ↑ UO
DIAGNOSTICS:
 ↓ Hgb and Hct
 ↓ Serum & urine osmolality
 ↓ Urine Na & specific gravity –
diluted urine
 Chest x-ray may reveal
pulmonary congestion
MEDICAL MANAGEMENT:
 Diuretics o Continuous renal
 Inhibits the reabsorption replacement therapy
of Na and H2O A special type of dialysis
 The choice of diuretics is that we do for unstable
based on: patients in the ICU whose
o Severity of the bodies cannot tolerate
hypervolemic state regular dialysis. Instead
o Degree of impairment of of doing it over four
renal function hours, CRRT is done 24
o Potency of the diuretic hours a day to slowly and
Pharmacologic Therapy continuously clean out
 Thiazide diuretics (potassium the waste products and
wasting) fluid from the patient.”
o Block Na reabsorption in
the distal convoluted
tubule(dct)
o Mild to moderate
hypervolemia
o Hydrochlorothiazide
 Loop diuretics (potassium
wasting)
o Block Na reabsorption in
the ascending limb of the
loop of Henle
o Severe hypervolemia
 Nutritional Therapy
o Furosemide (Lasix)
 Avoid foods high in Na
o bacon, sausage,
sardines, caviar
o pizza, burritos
o spam
o salted nuts
 o beans baseline first).
Sodium Salt contributes to edema.
Use lemon juice, onions, and garlic
(substitute flavoring).
 Salt substitutes
o Contains K (WOF
Hyperkalemia)
 K sparing diuretics
Advanced Kidney Disease
 Ammonium chloride
o harmful in patients with Support arms and legs to ↓
dependent edema
liver disease (hepatic
Other nursing mgt.
encephalopathy).
 Check for loc
Drinking water (1 mg or more than
 Maintain safety
1500 mg of sodium per quart)
 Positioning
 Distilled water (very high in Na)
 Na and fluid restriction
 Bottled water (0 to 1200 mg/L)
 Avoid OTC medications
 Water softener (↑ Na)
 Avoid water softeners
o Check the label before
 Avoid Parenteral fluids (with Na)
drinking
 Preventing skin breakdown
o ↑ Protein intake
o Slow healing process
NURSING MANAGEMENT:
o Turn and reposition at
Rest
regular intervals
 Bed rest favors diuresis of fluid
 Pulmonary edema
 ↑ In EFFECTIVE circulating
o Diuretics as ordered
blood volume and renal
perfusion  Educating patients about
 Diminished venous pooling edema
Vital Signs o Recognize and
 Note for BP understand edema
 Bounding pulse o Expansion of the
 Tachycardia interstitial fluid
Intake & Output compartment
 Done daily or at regular o ↑ Capillary fluid pressure
intervals to identify excessive  Dependent edema
fluid retention  Heart failure
Weight  Hypoproteinemia
 Measured daily  ↓ Capillary oncotic pressure
o lb. = 1 L of fluid  ↑ Interstitial oncotic pressure
Breath Sounds (pulmonary  Localized edema
edema/congestion) o Ankle, rheumatoid
 Assessed at regular intervals arthritis
o Crackles  Generalized edema
o Wheezing  Cardiac failure
o Diminished breath  Anasarca
sounds
Edema
 Monitor the degree of edema
o Feet and ankles
(ambulatory)
o Sacral region (supine/
bed-ridden)
o Pitting edema
 Medications that could cause
o Pressing a finger into the edema
affected part  NSAIDS
o Peripheral edema Inhibits natriuretic effect
o Measuring the (regulates excess fluid)
circumference of the  Estrogens
extremity (document
 Decreased blood flow in
the legs
 Corticosteroids
Has an anti-
inflammatory property
 Antihypertensives
Vasodilatory edema
 Ascites
o Fluid accumulates in the
peritoneal cavity BODY FLUID COMPUTATION
o Shortness of breath INTRACELLULAR FLUID COMPARTMENT
o Sense of pressure (ICF)
EXAMPLE: How much water is in the
intracellular fluid compartment (ICF)
of a 25-year-old male patient who
weighs 60 kg?

Step #1: Compute the total body

water (TBW) based on age and sex.
TBW = (60 kg) (0.6)
= 36 kg → weight of water
= 36 liters → volume of
water
Step #2: Compute for the intracellular
 Preserve or restore the fluid volume (67% of the total body
circulating intravascular fluid water is intracellular fluid)
volume ICF = (36 liters) (0.67)
o Diuretic therapy = 24.12 liters
o Restriction of fluids and
Na EXAMPLE: How much water is in the
o Elevation of the circulatory system of a 32-year-old
extremities female patient who weighs 52 kg?
o Application of anti-
embolism stockings Step #1: Compute the total body
o Paracentesis water based on age and sex.
o Dialysis TBW = (52 kg) (0.5)
o Continuous renal = 26 kg → weight of water
replacement therapy. = 26 liters → volume of
FLUID, ELECTROLYTE water
IMBALANCES Step #2: Compute the extracellular
FLUID BALANCE fluid volume (usually 33% of the total
 INTRACELLULAR FLUID body water).
COMPARTMENT (ICF) ECF = (26 liters) (0.33)
Fluid is found inside the cells. = 8.58 liters
It comprises 2/3 (67%) of the Step #3: Compute for the plasma
total body water. volume.
 EXTRACELLULAR FLUID Plasma = (9.6 liters)/3
COMPARTMENT (ECF) = 3.2 liters
Fluid is found outside the cells.
It comprises 1/3 (33%) of the
total body water.
One-third (1/3) of the ECF is in
plasma.

SERUM OSMOLARITY
 Reflects the amount of solute
particles in a solution and is a
 measure of the concentration of suctioning, draining fistulas
a given solution.  Edema, ascites, burns
 Can be calculated using the  Addison’s disease (Low
formula: aldosterone secretions)
(mg/dL) (mg/dL)
Glucose BUN

Na (2) + ___________ + ___________

18 3
(2, 18, & 3 are constant)
= Approximate Value of Serum
osmolality

Normal value = 275 – 290 mOsm/kg

 Sodium is the most active
determinant of serum
osmolality and is therefore
actively moved across
membranes to ensure normal
osmolality.
CLINICAL MANIFESTATIONS:
Normal value = 275 – (↓ECF and ↑ICF volume)
290mOsm/kg  Headache
 Sodium is the most active  Muscle weakness, fatigue and
determinant of serum apathy (lack of enthusiasm).
osmolality and is therefore  Anorexia, nausea and vomiting
actively moved across  Abdominal cramps
membranes to ensure normal  Weight loss
osmolality.  Postural hypotension
 Seizure, Coma
ELECTROLYTE IMBALANCES AND TREATMENT:
MANAGEMENT  Administration of NaCl 0.9% per
Sodium Imbalances IV, plasma expanders
Sodium (Na+) (135-145 meq/L) (hetastarch). To prevent shock.
 The primary extracellular cation  Sodium-rich foods in the diet
(+ charged). NURSING MANAGEMENT:
 Always accompanies water in  Identify and monitor patients at
the extracellular fluid risk for hyponatremia.
compartment.  Monitors I&O (identify excess
HYPONATREMIA water input or lack of sufficient
 Defined as serum sodium less water output) (+FV)
than 135 meq/L.  Daily body weight
 Most common electrolyte  Safety precautions (side rails,
abnormality observed in a supervision of ambulation)
general hospitalized population. HYPERNATREMIA
 Initial approach is the  Serum sodium greater than 145
determination of serum meq/L
osmolality  Develops from excess water
 It is caused by sodium loss or loss, frequently accompanied
water excess. by an impaired thirst
CAUSES: mechanism.
 Diuretics  Sodium and water excess
 Low sodium diet resulting in edema.
 Excessive ingestion of plain CAUSES:
water  Sodium tablets
 Profuse diaphoresis & diuresis  Hypokalemia, hypercalcemia, or
 Administration of electrolyte– sickle cell anemia can cause
free solution nephrogenic diabetes insipidus.
 Prolonged vomiting, GI  Hyperventilation
  Profuse watery diarrhea sodium.
EXAMPLE:
 Excessive salt intake without 1. A 32y/o 60kg male patient with
sufficient water intake hypernatremia with serum
 Decreased water intake sodium of Na+160 meq/L.
(elderly, debilitated, Step #2: Compute for the Volume to
unconscious clients) be replaced
 Excessive administration of = 36 x 160 – 140 = 36 x 20
solutions containing SODIUM 140 140
 Excessive water loss without
accompanying loss of sodium = 36 x .14285 (5 decimal
CLINICAL MANIFESTATIONS: places)
 (↑ECF and ↓ ICF volume: ICF =5.14 liters
Dehydration) NURSING MANAGEMENT:
 Extreme thirst  Fluid losses and gains are
 Dry, sticky mucous membranes carefully monitored in patients
 Oliguria at risk for hypernatremia.
 Firm, rubbery tissue turgor  Obtains a medication history (↑
 Fever sodium content)
 Rough, red, dry swollen tongue  Check for OTC medications (↑
 Lethargy sodium content)
 Restlessness, tachycardia,  Monitor I and O
fatigue  Restrict sodium diet
 Disorientation, hallucination  Administer diuretics as
 Coma if severe (Monitor GCS) prescribed.
CLINICAL FINDINGS:  Promote safety.
 Intact thirst mechanisms  Monitored closely for changes
usually prevent hypernatremia. in behavior, such as
 Its presence is commonly restlessness, disorientation, and
associated with encephalopathy lethargy.
of any cause or cerebrovascular HIGH IMPACT CONCEPT:
disease.  Hyponatremia
 Orthostatic hypotension and  Increase ICF Volume =
oliguria are typical (common). “Cell swell”
 Hyperthermia, delirium, and  Hypernatremia
coma may be seen as severe  Decrease ICF Volume =
hyperosmolality. “Cell shrink”
TREATMENT:
 Low sodium diet. Potassium Imbalances
 ↑ OFI or administer D5W per IV. Potassium (Na+) 3.5 – 5.0 meq/L
 Diuretics.  Major ICF cation
 Dialysis.  Regulates CHON synthesis,
 Directed toward correcting the glucose use & storage,
cause of the fluid loss and and maintains action potentials
replacing water and as needed, in excitable membranes.
electrolytes. HYPOKALEMIA
 IV administration of hypotonic  A total body deficit of about
solutions 350 meq occurs for each 1
CALCULATION OF WATER DEFICIT: meq/L decrement in serum
 When calculating fluid potassium concentration.
replacement, both the deficit  Changes in blood pH and
and the maintenance hormones (insulin, aldosterone,
requirement should be added to and β-adrenergic agonists)
each 24-hour replacement independently affect serum
regimen. potassium levels.
 Volume to be replaced
= current TBW x ([Na] – 140)
140 CAUSES:
140 & 140 are constant.  K+ wasting diuretics
Where [Na] is the measured serum
 (furosemide [Lasix], ethacrynic
acid [Edecrin],
hydrochlorothiazide
[HydroDIURIL]
 Severe vomiting & diarrhea,
draining intestinal fistula,
prolonged suctioning
 Large doses of corticosteroids
 IV administration of insulin &
glucose
 Prolonged administration of
non-electrolyte parenteral fluids CLINICAL MANIFESTATIONS:
CLINICAL MANIFESTATIONS:  Kidney:
Note: Due to ↓ neuromuscular o Water loss
irritability o Thirst
 GI Tract: o Renal damage
o Anorexia Note: Hypokalemia also increases the
o Nausea & Vomiting likelihood of digitalis toxicity
o Abdominal distention  ECG changes
o Paralytic ileus (non- o ST-segment depression
mechanical obstruction) o Flat or inverted T-wave
 CNS: o Increased U-wave
o Lethargy
o Diminished deep tendon
reflexes (hyporeflexia)
o Confusion
o Mental depression
 Muscle:
o Weakness TREATMENT:
o Fatigue  Elimination of the cause
o Leg cramps  Substitute K-wasting with K-
sparing diuretics
o Flaccid paralysis
(Spironolactone [Aldactone]
o Weakness of respiratory
 Increase oral intake of K-rich
muscles foods/ K supplements (Safest
o Tetany and way) (mild cases)
rhabdomyolysis  Intravenous replacement is
o Respiratory arrest indicated for patients with
 Cardiovascular system: severe hypokalemia.
o Hypotension  If serum potassium is > 2.5
o Dysrhythmias meq/L, and there are no ECG
o Myocardial damage abnormalities, potassium can
o Cardiac arrest be given at a rate of 10
meq/L/hr. in concentration that
TETANY – hyperexcitability /abnormnal should never exceed 40 meq/L.
muscle contraction.  For severe deficiency,
potassium may be given
through a peripheral
intravenous line at a rate of up
to 40 meq/L/hr.
 Occasionally, hypokalemia may
be refractory to potassium
replacement. Magnesium
deficiency may make potassium
correction more difficult.
Concomitant magnesium
repletion avoids this problem.
RHABDOMYOLYSIS – breakdown of
muscle triggering potassium excretion
 CLINICAL MANIFESTATIONS:
NURSING MANAGEMENT: Note: Due to ↑ neuromuscular
 Monitor for its early presence in irritability
patients at risk.  GI Tract:
o Fatigue, anorexia, muscle o Nausea & Vomiting
weakness, decreased o Diarrhea
bowel motility, o Colic
paresthesia, and  CNS:
arrhythmias are signals o Numbness
that warrant assessing o Tingling
the serum potassium  Muscle
concentration. o Irritability (Early)
 monitored closely for signs of o Weakness (Late)
digitalis toxicity. o Flaccid paralysis
NURSING ALERT!!!  Cardiovascular:
 NEVER administer Potassium o Ventricular fibrillation
Chloride (KCl) per IV push or
o Cardiac arrest
direct IV.
 Kidney:
This may cause dysrhythmias and
o Oliguria -decreased urine
cardiac arrest.
 “No pee No potassium” (UO output
>30ml/Hr.) to prevent renal o Anuria -absence of urine
damage. output
 KCL to IV should not exceed CLINICAL FINDINGS:
60mEq/L (preferred level:  Peak T waves
30mEq/L)  Prolonged PR intervals
 Rate should not exceed 10-  Flat or absent P wave
20mEq/ Hr. to prevent  Wide QRS complex
hyperkalemia and cardiac
arrest.
 Use Infusion Pump
HIGH IMPACT CONCEPT:
 Decreased neuromuscular
irritability
 “Everything is low and slow”
HYPERKALEMIA TREATMENT:
 Many are spurious (false/fake)  Confirm that the elevated level
or associated with acidosis. of serum potassium is genuine.
 Common practice of repeatedly  Measure plasma potassium.
clenching and unclenching the  Withholding of potassium.
fist during venipuncture may  Giving cation exchange resins
raise the potassium by mouth or enema:
concentration by 1-2 meq/L by polystyrene sulfate, 40-80
causing local release of muscles g/day in divided doses.
from forearm muscles.  Emergent treatment is
indicated if cardiac toxicity or
muscular paralysis is present,
or if hyperkalemia is severe
(>6.5-7 meq/L) even in the
absence of ECG changes.
(Administer D50-50 / glucose)
 Insulin plus 10-50% glucose
 may be employed to deposit
potassium with glycogen in the HYPOCALCEMIA
liver.  Seen commonly in critically ill
 Calcium gluconate per IV may patients due to acquired
be given intravenously as an defects in the parathyroid-
antagonist ion. (Antidote for vitamin D axis.
hyperkalemia)  Results occasionally in
 Stimulate transcellular shifts by hypotension which responds to
giving beta-adrenergic agonist calcium replacement therapy.
drugs.
 Sodium bicarbonate is an CAUSES:
emergency measure.  Decrease dietary intake
 Hemodialysis or peritoneal  Excess loss of calcium (renal
dialysis. disease, draining fistula)
NURSING MANAGEMENT:  ↓ Calcium absorption (Vit D
 Encouraging the patient to deficiency,
adhere to the prescribed Hypoparathyroidism,
potassium restriction. hyperthyroidism,
 Potassium-rich foods to be hypermagnesemia)
avoided include many fruits and  Acute pancreatitis
vegetables, legumes, whole-  Corticosteroids
grain breads, lean meat, milk,  Rapid administration of multiple
eggs, coffee, tea, and cocoa. units of blood that contain an
 Check labels of cola beverages anti-calcium additive (3 bags of
(↑ K+) PRBC or more or calcium
 Monitors I&O and observes for gluconate)
signs of muscle weakness and  Intestinal malabsorption
arrhythmias.  Accidental removal of
 When measuring vital signs, an parathyroid glands
apical pulse should be taken. CLINICAL MANIFESTATION:
HIGH IMPACT CONCEPT: Note: ↑ cell membrane permeability
 Increased neuromuscular = ↑ neuromuscular irritability
irritability  Central nervous system:
 “Everything is high and fast” o Tingling (paresthesia)
 The main route for potassium o Convulsions
excretion is the kidneys  Gastrointestinal tract:
o Increased peristalsis
Calcium Imbalances o Nausea and vomiting
Calcium (Ca++) 8.5 – 10.5 mg/dL o Diarrhea
 Bone strength & density, o Abdominal Pain
activation of enzymes or  Muscles:
reactions, skeletal/ cardiac o Muscle spasm
muscle contraction, nerve o Laryngospasm with
impulse transmission, blood
stridor
clotting.
o Tetany (Chvostek's sign
 Constitute 2% of body weight,
and Trousseau's sign)
but only 1% of the total body
 Cardiovascular system:
calcium is in solution in body
o Dysrhythmias,
fluid.
o Cardiac arrest.
 In plasma, calcium is present as
a non-diffusible complex with Other signs and symptoms:
protein (33%); as a diffusible  Bones:
but undissociated complex with o Osteoporosis
anions like citrate, bicarbonate, o Fracture (these are due
and phosphate (12%); and as to decreased calcium
ionized calcium (55%). deposited into the bones)
 It is the ionized calcium that is LABORATORY FINDINGS:
necessary for muscle  Low serum calcium
contraction and nerve function  Elevated serum phosphorus
(normal: 4.7 to 5.3 mg/dL).  Low serum magnesium
  Prolonged QT interval on the leukemia, lymphomas)
ECG CLINICAL MANIFESTATIONS :
TREATMENT: Note: ↓ cell membrane permeability
Asymptomatic hypocalcemia: = ↓ neuromuscular irritability
 High Calcium diet  Central nervous system:
 Oral calcium and vitamin D o Diminished deep-tendon
preparations. reflexes
 Calcium carbonate is well o Lethargy
tolerated and inexpensive. o Mental changes
Severe symptomatic hypocalcemia (decreased memory &
 In the presence of tetany, attention span)
arrhythmias, or seizures, o Coma (monitor GCS)
calcium gluconate 10% is  Gastrointestinal tract:
administered intravenously for o Decreased peristalsis
10-15 minutes or via calcium (constipation, paralytic
infusion (to avoid hypotension ileus).
caused by vasodilation). o Anorexia
 10-15 mg of calcium per o Nausea & vomiting
kilogram body weight, or 6-8  Muscles:
10-ml vials of 10% calcium o Muscle fatigue
gluconate (558-744 mg
o Hypotonia
calcium) is added to 1 liter of
 Cardiovascular system:
D5W and infused over 4 to 6
o Depressed electrical
hours.
activity (dysrhythmias)
NURSING MANAGEMENT:
o Cardiac arrest
 Closely monitor for neurologic
manifestations (tetany, Other signs and symptoms:
seizures, spasms)  Bones:
 Seizure precautions (side rails o Deep bone pain
up with pillows & ambulate with o Osteoporosis
assistance) o Pathologic fractures
 Provide bed rest for comfort,  Kidneys:
avoid falls (Prevent fracture) o Thirst
 Cardiac dysrhythmia & airway o Polyuria
obstruction o Dehydration
 Monitor breathing o Stones
(laryngospasm) -stridor o Renal damage
 Check for signs of bruising or TREATMENT:
bleeding  Determining & correcting the
HIGH IMPACT CONCEPT: cause
 Increase fluid intake(3-4L/day) -
prevention of kidney stone
formation
 Limit Ca++ consumption (mild
cases)
 Provide acid-ash fruit juice
(Cranberry & prune juice) and
vitamin C -kidney stone
HYPERCALCEMIA prevention
CAUSES:  0.45% or 0.9%NaCL (acute
 Excessive intake of calcium cases) and diuretics:
 Excessive doses of vitamin D furosemide (Lasix); oral
 Calcium loss from bone phosphates; calcitonin
(Immobilization, carcinoma with (Cibacalcin)
bone metastases)  Corticosteroids or plicamycin
 Parathyroid gland tumors (Mithracin) – used for malignant
 Multiple fractures diseases that do not respond to
 Hyperparathyroidism other forms of therapy
 Certain malignant diseases NURSING MANAGEMENT:
(multiple myeloma, acute  Encourage increased fluid
 intake acetylcholine release.
 Encourage high fiber diet  Central nervous system:
 Collaborates with a dietitian to o Convulsions -involuntary
limit food sources of Ca++ contraction of muscles
 Ambulation is tolerated. o Paresthesia -tingling of
(prevent hypercalcemia or fingers and toes
minimize severity) o Tremors
 Provide assistance; avoid falls o Ataxia
 Increased calcium increases the o Athetoid movements
effects of digitalis (WOF o Jerking
Toxicity) o Nystagmus -involuntary
 Monitor cardiac rate and eye movement
rhythm for any abnormalities.  Mental changes:
HIGH IMPACT CONCEPT: o Agitation
o Depression
o Confusion and
disorientation
 Muscles:
o Weakness
o Cramps
o Spasticity
Magnesium Imbalances o Tetany
Magnesium (Mg++) 1.8 - 3.6 mg/dL  Cardiovascular system:
 About 50% of total body o Tachycardia
magnesium exists in the o Hypertension
insoluble state in bone. o Dysrhythmia
 Only 5% is present as  Positive Babinski response -
extracellular cation; the the extension of big toe +
remaining 45% is contained in abduction of other toes
cells as intracellular cation. LABORATORY FINDINGS:
 Normal plasma concentration is  Decreased serum magnesium
1.5-2.5 meq/L, with about one- levels
third bound to protein and two-  Hypocalcemia and hypokalemia
thirds existing as free cation.  Prolonged QT interval on the
 Excretion is via the kidney. ECG
HYPOMAGNESEMIA  Lengthening of the ST segment
 Nearly half of hospitalized on the ECG
patients have unrecognized TREATMENT:
hypomagnesemia.  Magnesium-rich diet
 In critically ill patients,  Use of IVF containing
arrhythmias and sudden death magnesium as chloride or
may be complications. sulfate, 240-1200 mg/day (10-
CAUSES: 50 mmol/day) during the period
 Chronic alcoholism of severe deficit, followed by
 Severe renal disease 120 mg/day (5 mmol/day) for
 Severe malnutrition or maintenance.
starvation  MgSO4 may also be given
 Intestinal malabsorption intramuscularly in a dosage of
syndromes 200-800 mg/day
 Excessive diuresis (drug- (8-33mmol/day) in four divided
induced) -due to use of doses.
diuretics  Serum levels must be
 Prolonged gastric suction monitored.
 Draining fistula NURSING MANAGEMENT:
CLINICAL MANIFESTATIONS:  Encourage and provide food
Note: magnesium inhibits rich in magnesium
acetylcholine (neurotransmitter for  Promote safety and protect
brain function) release. Therefore, in clients from injury.
hypomagnesemia, there is increased  Monitor for laryngeal
 stridor(spasm). (Airway  Administration of fluids and
obstruction) diuretics
 Administer magnesium oral  Administration of calcium
supplements or IV as gluconate per IV as prescribed.
prescribed. (antagonize magnesium)
 If you’re giving MgSO4, always  Hemodialysis or peritoneal
check the BP!!! (vasodilation) dialysis
HIGH IMPACT CONCEPT: NURSING MANAGEMENT:
 Closely observe for
dysrhythmias (apical) & early
signs of neuromuscular
irritability
 Antidote: Calcium gluconate
(kept available)
 Monitoring of I&O
 Monitor vital signs (hypotension
HYPERMAGNESEMIA and shallow respirations)
 Almost always the result of  Provide health teaching
renal insufficiency and the Phosphorous Imbalances
inability to excrete what has Phosphorus (P) 2.5 – 4.5 mg/dL
been taken in from food or  Activating B-complex vitamins,
drugs, especially antacids and ATP(energy), assisting in cell
laxatives. division, cooperating in CHO,
 Potentially life-threatening as it CHON & FAT metabolism, acid-
impairs both the central base buffering, calcium
nervous system and muscular homeostasis; balanced &
function. reciprocal relationship w/ Ca++
CAUSES: HYPOPHOSPHATEMIA
 Excessive intake of magnesium- CAUSES:
containing antacids  Inadequate intake
 Renal failure  GI malabsorption disorders
 DKA -Diabetic Ketoacidosis (chronic, diarrhea, Crohn’s
CLINICAL MANIFESTATIONS: disease – large intestine, or
Note: Magnesium inhibits Celiac disease – small
acetylcholine release. Therefore, in intestine).
hypermagnesemia, there is decreased  Anorexia (starvation)& bulimia
acetylcholine release (binge-eating then purging)
 Decreased BP  Alcoholism.
 Thirst  Vitamin D deficit (causes low
 nausea and vomiting phosphate levels in the
 Drowsiness bloodstream).
 Diminished or loss of deep  High intake of antacids.
tendon reflexes.  Heatstroke
 Muscle weakness  Prolonged intense
 Mental obtundation and hyperventilation
confusion  Alcohol withdrawal
 Respiratory muscle paralysis or  DKA
cardiac arrest – respiratory  Respiratory alkalosis
failure  Hepatic encephalopathy
LABORATORY FINDINGS:  Major thermal burns
 Elevated serum magnesium,  Hyperparathyroidism
BUN, creatinine, K CLINICAL MANIFESTATIONS:
 Decreased serum calcium  Tissue hypoxia – phosphate is
 Increased PR interval on the needed to bind oxygen to blood
ECG circulation
 Broadened QRS complex with  Increased susceptibility to
elevated T waves infection
TREATMENT:  Nystagmus
 Correct underlying cause. TREATMENT:
 Alleviating renal insufficiency  Prevention of
 hypophosphatemia is the goal. urinary phosphate excretion)
 Oral phosphate supplements  high phosphate intake
(mild hypophosphatemia, renal-  Shift of phosphate from the ICF
wasting disorders, to ECF.
malabsorption, or oncogenic  Excessive vitamin D intake
osteomalacia)  TPN
 Vitamin D may (enhance  Hypoparathyroidism - ↓PTH =
absorption of phosphorus and ↑Phosphate and ↓Calcium
calcium).  Metabolic or respiratory
 IV phosphorus correction is acidosis
usually limited to the patient  DKA
whose serum phosphorus levels CLINICAL MANIFESTATIONS:
decrease to less than 1 mg/dL Note: Most symptoms result from
(0.3 mmol/L). decreased calcium levels and soft
 Prevention of tissue calcifications.
hypophosphatemia is the goal.  Tetany
 Oral phosphate supplements  Tachycardia
(mild hypophosphatemia, renal-  Anorexia
wasting disorders,  Nausea and vomiting
malabsorption, or oncogenic  Muscle weakness
osteomalacia)  Signs and symptoms of
 Vitamin D may (enhance hypocalcemia
absorption of phosphorus and  Hyperactive reflexes
calcium).  Soft tissue calcifications in
 IV phosphorus correction is lungs, heart, kidneys, and
usually limited to the patient cornea
whose serum phosphorus levels TREATMENT:
decrease to less than 1 mg/dL  Phosphate intake should be
(0.3 mmol/L). reduced, and phosphate
 Monoclonal antibody-type drug, binders can be given with
burosumab, (renal phosphate meals to reduce
wasting disorders and hyperphosphatemia.
hypophosphatemic rickets)  Treatment of underlying
NURSING MANAGEMENT: disorder.
 TPN (total Parenteral Nutrition):  Calcium carbonate or calcium
gradually introducing the citrate are (to lower blood
solution to avoid rapid shifts of phosphate levels). WOF
phosphorus into the cells. hypercalcemia
 Frequently monitors serum  Sevelamer and lanthanum (Not
phosphorus levels and containing calcium)
documents and reports early  Sucroferric oxyhydroxide (iron
signs of hypophosphatemia supplementation)
(apprehension, confusion,  Forced diuresis with a loop
change in level of diuretic or saline diuresis can
consciousness). be used in patients with normal
 Encouraged intake of milk and renal function.
milk products, organ meats,  Hemodialysis
beans, nuts, fish, poultry, and NURSING MANAGEMENT:
whole grains.  Instructed to avoid phosphorus-
 IV preparations of phosphorus: rich foods, such as hard
the rate of phosphorus cheeses, cream, nuts, meats,
administration should not whole-grain cereals, dried
exceed 3 mmol/h, monitor the fruits, dried vegetables,
IV site regularly to prevent kidneys, sardines, and dairy
tissue sloughing and necrosis foods.
due to  monitors urine output during
infiltration(extravasation). diuresis
HYPERPHOSPHATEMIA  Educates the patient about
CAUSES: recognizing the signs of
 Kidney injury (diminishes hypocalcemia, such as muscle
 cramping.  Kussmaul’s breathing (Deep,
rapid breathing which is an
ACID-BASE IMBALANCES attempt to blow off CO2)
Body fluids contain ACIDS & BASES  Hyperkalemia
aside from electrolytes  CNS depression
 H2CO3 (Carbonic) acid & base DIAGNOSTICS:
content influence the pH  ABG analysis
 HCO3 (bicarbonate) of the body  Hyperkalemia
(amount of H+ in a solution)  ECG: Tall Peaked T-wave
Regulation of pH is accomplished by: MEDICAL/NURSING MANAGEMENT:
 Buffer systems  Maintain good respiratory
o REMOVE or RELEASE function.
hydrogen ion (acid)  Fluid replacement. Water loss
o Excessive hydrogen ion may result from
(ACIDOSIS) ↑hydrogen hyperventilation.
ion → BUFFERS BIND  Protect the client from injury.
o Decrease in hydrogen ion Risk for injury related to mental
(ALKALOSIS) ↓hydrogen dullness (↓memory &
ion→ BUFFERS RELEASE ↓cognitive skills).
hydrogen ion  Restore electrolyte balance,
 Kidneys specifically potassium.
Renal Regulation  Administer Sodium
o ELIMINATES or RETAINS Bicarbonate )alkaline/base) per
HCO3 IV as prescribed.
o ELIMINATES or RETAINS  Identify and treat underlying
hydrogen ion causes, e.g., renal failure, DM,
starvation ketoacidosis (DKA),
shock, chronic diarrhea, ASA
poisoning (acetyl salicylic
acid/aspirin).
 Hemo/peritoneal dialysis
 Lungs
Respiratory Regulation
METABOLIC ALKALOSIS
o RETAINS or ELIMINATES
Bicarbonate Excess
Carbon Dioxide (potential
 Result from loss of hydrogen ion
acid)
or addition of base to body
fluid.
CAUSES:
 Gain of bicarbonate (HCO3)
o Alkali intake
 Loss of hydrogen ion
METABOLIC ACIDOSIS o Vomiting – HCL
Bicarbonate Deficit (hydrochloric acid)
 Result from abnormal o Suction
accumulation of fixed acids or  Loss of potassium
loss of base. o Diuretics
CAUSES: CLINICAL MANIFESTATIONS:
Loss of bicarbonate (HCO3)  Hypoventilation (the body's
 Intestinal loss - diarrhea attempt to conserve CO2)
 Diuretics  Mental confusion
Accumulation of acids  Dizziness
 Lactic acid  Numbness and tingling of
 Ketoacids -DKA fingers and toes
 Uremia/Azote - ↑urea  Muscle twitching, tetany, and
 Salicylate poisoning – ASA seizures (these are due to
(aspirin) hypocalcemia because alkalosis
CLINICAL MANIFESTATIONS: damages ionized calcium)
 Headache  Potassium deficit
 Mental dullness (hypokalemia).
 ↑RR – CO2
 o Decreased GI motility (hyperkalemia)
and paralytic ileus DIAGNOSTICS:
o ECG: extra “U” wave  ABG analysis
DIAGNOSTICS:  Hyperkalemia
 ABG analysis  ECG: Tall-peaked T-wave (V-fib)
 Hypokalemia = Hypocalcemia MEDICAL/NURSING MANAGEMENT:
 ECG: Extra “U” wave  Correct underlying cause
MEDICAL/NURSING MANAGEMENT:  Bronchodilator
 Maintain good respiratory  Postural drainage
function.  Semi-fowler’s position
 Protect the client from injury.  Chest clapping
Seizures may occur.  Na Bicarbonate for ventricular
 NaCl or Ammonium Chloride fibrillation or potassium excess
oral or intravenous.
 KCL (potassium chloride) RESPIRATORY ALKALOSIS
infusion Carbonic Acid Deficit
 Diamox (Acetazolamide). This is  Loss of CO2 from the lungs at a
a carbonic anhydrase inhibitor faster rate than it is produced in
that increases the excretion of the tissue
bicarbonate by the kidneys. CAUSES:
 Identify and treat underlying  Hyperventilation
causes, e.g., excessive intake of  EXCESSIVE release of Carbon
sodium bicarbonate or baking dioxide in the LUNGS
soda, vomiting, gastric  Anxiety, Fever, Meningitis
suctioning, intestinal fistulas.  ASA Poisoning
 Avoid antacids  Pneumonia
 Anti-emetics  Pulmonary Embolism
CLINICAL MANIFESTATIONS:
RESPIRATORY ACIDOSIS  Lightheadedness
Carbonic Acid Excess  Numbness or tingling of fingers
 Failure of the respiratory or toes (hypocalcemia)
system to remove CO2 from  Late: tetany convulsions
body fluids as fast as it is  Hyperpnea (tachypnea)
produced in the tissue. (increased RR and depth)
CAUSES:  Potassium deficit (hypokalemia)
 Hyperventilation DIAGNOSTICS:
 DISORDERS that restrict/limit  ABG analysis
the RELEASE of Carbon dioxide  Hypokalemia
in the LUNGS  hypocalcemia
o COPD MEDICAL/NURSING MANAGEMENT:
o Impaired movement of  Correct underlying cause
Thoracic Cage  BROWN BAG
o Depressed respiratory  Slow breathing
center  Purse-lip breathing
o Neuromuscular disease RESPIRATORY ACID-BASE
CLINICAL MANIFESTATIONS: IMBALANCE CYCLE
 Tachypnea (increased RR and
depth)
 Tachycardia
 Visual disturbances
 Headaches, restlessness
 Drowsiness, confusion
 Diaphoresis
 Ventricular fibrillation
 Cyanosis (hypoxia)
 Late: confusion, drowsiness,
coma
 Increased ICP (severe)
 Potassium excess
 HCO3 22 - 26
CONCEPT METHOD

PaCO2 = ABNORMAL

HCO3 = NORMAL
=
Information obtained from the arterial RESPIRATORY
blood gas measurements:
 pH PaCO2 = NORMAL
 Partial pressure of carbon
dioxide (PaCO2)
HCO3 = ABNORMAL
 Partial pressure of oxygen
=
(PaO2)
METABOLIC
 HCO3 level
EXAMPLES:
 Oxygen saturation (O2Sat)
PH = 7.25 PaCO2 = 37
Normal values:
HCO3 = 21
 pH = 7.35 – 7.45
ACIDOSIS NORMAL
 PaCO2 = 35 – 45 mmHg
ABNORMAL
 PaO2 = 80 – 100 mmHg
METABOLIC ACIDOSIS
 HCO3 = 22 – 26 meqs/L
UNCOMPENSATED
 O2Sat > 95%-100%
ABG INTERPRETATION
PH = 7.56 PaCO2 = 40 HCO3 =
35
ALKALOSIS NORMAL
ABNORMAL
METABOLIC ALKALOSIS
UNCOMPENSATED

ABG INTERPRETATION NORMAL PH = 7.56 PaCO2 = 30 HCO3 =

VALUES 35
ALKALOSIS ABNORMAL NORMAL
RESPIRATORY ALKALOSIS
UNCOMPENSATED

3. Identify if it is uncompensated
or compensated (Partial or
Fully).
ABG INTERPRETATION
 Full Compensation
 Partial Compensation

COMPENSATION
RESPIRATORY
Acidosis Alkalosis
3 STEPS ABG INTERPRETATION HCO3 ↑ 26 ↓ 22
1. Identify if it is acidosis or
alkalosis (PH). METABOLIC
NORMAL VALUE: PH 7.35 – 7.45 Acidosis Alkalosis
Less than 7.35 = Acidosis CO2 ↓ 35 ↑ 45
Greater than 7.45 = Alkalosis
Example: Relation to:
PH 7.25 =ACIDOSIS PaCO2
PH 7.55 = ALKALOSIS = ↑Carbon dioxide = ACID = Acidosis
2. Identify if it is respiratory or ↓Carbon dioxide = BASE =
metabolic (CO2/HCO3). Alkalosis
NORMAL VALUES: PaCO2 35 - 45 / HCO3
= ↑Bicarbonate = BASE = Alkalosis exposure to excessive heat.
↓Bicarbonate = ACID = Acidosis  Traumatic injury to the skin and
underlying tissues caused by
NORMAL VALUE: PH 7.35 – 7.45 heat, chemical, & electrical
injuries (most severe!!!)
NORMAL PH = FULL COMPENSATION degree of tissue damage is related to:
ABNORMAL PH = PARTIAL  What agent caused the burn
COMPENSATION  Temperature of the burning
agent
EXAMPLES:  Duration of contact with the
PH = 7.30 Respiratory agent
Acidosis  Thickness of the skin
PaCO2 = 50 (Acid) TYPES OF BURN ETIOLOGY
HCO3 = 49 PARTIAL Thermal Burns
Compensation  Dry heat – flames, hot objects
Chemical Burns
PH = 7.50 Metabolic Alkalosis  Acids, alkali
PaCO2 = 51 PARTIAL Smoke and Inhalation injury
Compensation  Carbon monoxide poisoning,
HCO3 = 41 (Base) hot air, steam/smoke
Radiation Burns
IF PH is normal but PaCO2 is elevated  Ionizing radiation e.g., nuclear
(Acid) and HCO3 is elevated (Base) energy, radiation therapy
How to identify Acidity or Alkalinity? Cold Thermal Injury (frostbite)
1. Know your patient's Diagnosis  Prolong exposure to cold.
If Lung related problem (retaining Electrical Burns
CO2)  Electric current
= Respiratory Acidosis  Muscle contractions (Fracture)
If Diarrhea or vomiting (losing Acid)  Risk for cervical spine injury
= Metabolic Alkalosis (Fall)
2. Use the Acidic side/Alkalotic  Electrical burn: internal damage
side method a. CNS complications,
NORMAL: ACIDOSIS OR ALKALOSIS b. Cardiac dysrhythmia,
(N)ACIDIC SIDE c. Cardiac arrest,
(N)ALKALOTIC SIDE d. Severe metabolic acidosis,
7.35, 7.36, 7.37, 7.38, 7.39 40 7.41, 7.42, 7.43, e. Myoglobinuria = acute tubular
7.44, 7.45
necrosis
EXAMPLE:
PH = 7.35
Respiratory(N)Acidosis
PaCO2 = 59 (Acid)
HCO3 = 30 FULL
Compensation
PH = 7.44
Metabolic(N)Alkalosis
PaCO2 = 50 FULL
Compensation
HCO3 = 49 (Base)
RISK FOR MORTALITY: 90%
BURN INJURY  >60y/o
 >40% of T.S.B.A.
Burns
 Presence of inhalation injury
Burns is one of the most devastating
experiences that a human individual
could ever have, especially in cases of
severe burns. It affects the
physiologic, psychologic, social,
economic, and spiritual aspects of a
person's life.
 Tissue damage caused by
 Partial-thickness wound
 Entire epidermis & varying
depths of the dermis
 2 types:
 Superficial partial
thickness
 Deep partial thickness
Superficial partial-thickness
wound
 There is the involvement of the
upper 3rd of the dermis leaving
a good blood supply; wounds
are red, moist & blanch (white)
when pressure is applied
 Blister formation (leakage of
a large amount of plasma from
DEPTH OF BURN INJURY
the injured small vessels lifting
off the destroyed epidermis)
 Intense pain due to exposed
nerve endings especially when
stimulated by touch &
temperature changes
 with standard care, heals in 10-
21 days with no scar, but some
minor pigment changes may
occur

Superficial-thickness wounds
 The epidermis is the only part
injured.
 desquamation occurs for 2-3
days after the burn heals in 3-5
days without a scar or
complications
e.g., sunburn, short (flash)
exposure to high-intensity heat
 healing can take from weeks to
months depending on the
establishment of a good blood
supply to the injured areas

Deep partial-thickness wound

 wounds that extend deeper into
the skin, dermis and fewer
healthy cells remain; wounds
are red & dry (because fewer
blood vessels are patent) with
white areas in deeper parts due
to ischemia, hypoxia & even Deep full-thickness wound
infection can progress to full-  wounds that extend beyond the
thickness wounds skin into underlying fascia &
 No Blister formation because tissues
the dead tissue layer is so thick  damages the muscle, bone, and
& sticks to the underlying tendons & leave them exposed
viable dermis that it does not  wound is blackened and
readily lift off the surface depressed, and sensation is
 Lesser degree of pain (more completely absent
nerve endings have been
destroyed), moderate edema is
present, generally heals in 3-6
weeks with scar formation

Full-thickness wound
 destruction of the entire
epidermis & dermis, leaving no
residual epidermal cells to
repopulate; wound may be
waxy, white, deep red, yellow,
brown or black, hard, dry,
leathery eschar (burn crust)
[eschar is a dead tissue; it must
slough off or be removed from
the burn wound before healing
can occur]
 avascular, no sensation or
OTHER INJURIES INCURRED WITH
BURNS:
 Fractures
 Major Soft Tissue Damage
 Respiratory distress (Critical)
 Increase ICP – Cerebral damage
PRE-EXISTING MEDICAL SURGICAL
CONDITIONS:
 DM – Diabetes Mellitus
 CAD – Coronary Artery Disease
 COPD – Chronic Obstructive
Pulmonary Disease
 CRF -
 Buerger’s (P.V.D.)
CLASSIFICATION OF SEVERITY
Minor Burns
 P.T.B. < 15% T.S.B.A.
 F.T.B. < 2% T.S.B.A.
 Need no Hospitalization and IVF
replacement treated on an
outpatient basis.
Moderate Burns
 P.T.B. > 15%, < 25-30% T.S.B.A.
 F.T.B. > 2%, 10% T.S.B.A.
provided that face, feet, hands,
neck, and genitalia are NOT
INVOLVED
Critical Burns
 Partial thickness burns > 25-
30% T.S.B.A.
 Full thickness burns > 10%
T.S.B.A.
 Burns complicated by:
a. Respiratory distress
b. Fractures
c. Major soft tissue damage
>Cerebral contusions – increase
ICP
>Spleen, kidney, liver damage
>Bleeding
All electrical burns
THE STAGES OF BURN
1. The first stage of burns is called
the Shock Phase or Fluid
Accumulation Phase or
Emergent Phase.
 It occurs during the first 48
 hours of post-burns. excretion of bicarbonate by the
 Fluid shifts from kidneys.
the intravascular compartment 3. The third stage of the burns is
to the interstitial compartment the Recovery Stage.
(IVC to ISC). This leads to  This occurs on the 5th day,
dehydration. onwards.
 Hypovolemia occurs due to  The following problems occur
plasma loss. This causes during this time:
decreased cardiac output and  Hypocalcemia. This results
a fall in BP. from the loss of calcium in the
 Hemoconcentration, exudates. It is also due to
increased hematocrit. the utilization of calcium in the
Plasma is lost into the granulation tissue (scar)
interstitial compartment (ISC). formation in the areas of burns.
 Oliguria. This is due to
decreased renal tissue  Negative nitrogen balance.
perfusion, and increased In stress-like burns, there is
release of ADH and aldosterone. increased protein catabolism.
These are the body's responses Protein demands are increased
to hypovolemia. for healing and protein intake
 Hyperkalemia and may be inadequate.
hyponatremia. This results  Hypokalemia. Potassium has
from the release of potassium shifted back into the cells;
from damaged cells; sodium is serum levels are decreased.
trapped in the edema fluids FIRST-AID INTERVENTION FOR BURNS:
(ISC). Stop the burning process
 Metabolic acidosis. This 1. Immerse the affected part in
results from the accumulation cold water.
of metabolites, hyponatremia, 2. "Drop and roll." Advise the
and hyperkalemia. Primarily, it client to drop and roll on the
is due to hyponatremia. Since ground if clothing is in flame. To
sodium is unavailable because smother the flame.
it is trapped in the edema 3. Throw a blanket over the
fluids, bicarbonate produced by client to extinguish the flame.
the kidneys will be excreted. This cuts off the source of
2. The second stage of burns is oxygen from the environment
called the Diuretic or Fluid and the flame will
Remobilization phase. spontaneously be extinguished.
 This occurs after 48 hours of The priority actions in case of fire are
post burns. as follows:
 Fluid shifts from the interstitial Remove the patient
compartment to Activate the fire alarm
the intravascular compartment Confine the fire.
(ISC to IVC). Extinguish the fire
 Hypervolemia, To use the fire extinguisher, do the
hemodilution, and following:
decreased hematocrit occur. Twist the pin to break the safety seal
This is due to the fluid shift Pull the pin
from ISC to IVC. Aim at the base of the flame
 Diuresis. This is due to Squeeze the handle
increased renal tissue Sweep from side to side
perfusion, decreased ADH, and LOCATION OF BURNS
aldosterone secretion.  Head, Neck Face – smoke
 Hypokalemia, inhalation, respiratory
hyponatremia. Potassium obstruction, cosmetic problem.
moves back into the cells;  Ears – decrease blood supply –
sodium is still trapped in the increase infections.
edema fluids.  Hands and feet – abundant
 Metabolic acidosis. blood and nerve supply
Decreased sodium levels cause  nerve supply
  blood volume and ages.
contractures
 severe limit.
 Joints - deformities; decrease
ROM
 Genitalia – urethral stricture,
decreased sensitivity
 Circumferential burns of
the chest – restriction of
breathing
CRITERIA FOR NURSING ASSESSMENT
Total Surface of Burned Area
(T.S.B.A.)
 Determines the extent of
damage
 Uses assessment guides such
as Rule of Nines, Lund and
Browder Chart, Berkow Method,
and Palm method
RULE OF NINES
 Head and Neck = 9%
 Upper extremities = 9% PALM METHOD
of each arm (total 18%)  The most practical method
 Lower extremities = 18% employed in patients with
of each leg (total 36%) scattered burns
 Anterior Trunk = 18%  The size of the palm of the
 Posterior trunk = 18% PATIENT (not the examiner’s) is
 Genitalia = 1% approximately 1% of the TBSA
 TOTAL =
100%

FLUID REPLACEMENT
To prevent hypovolemic shock.
Types of fluid replacement:
 Colloids: blood, plasma
expanders (e.g. Hetastarch)
 Electrolytes: Lactated Ringers
(LR)
 Non-electrolytes: Dextrose
5% in water (D5W)
BAXTER AND PARKLAND
FORMULA (Crystallized
Resuscitation)
LUND AND BROWDER CHART 4mls. LR x weight in kg. x %
T.S.B.A
Allocation of fluid replacement for the
first 24 hours:
1st 8 hours: 50%
2nd 8 hours: 25%
3rd 8 hours: 25%
SPECIAL CHARTS & GRAPHS EXAMPLE: A client weight 90kg and
(BERKOW METHOD) percentage of body burns is 22%.
 More accurate for evaluating Total Volume of Fluid Replacement:
the size of the injury 4mls X 90kg. X 22% = 7,920
 Uses a diagram of the body mls.
divided into sections, with the 1st 8 hours: 50% = 7,920 mls. X
representative % of TBSA for all 0.50
 3,960 mls.  The Rule of 9's for determining
2nd 8 hours: 25% = 1,980 mls. the percentage of burns in an
3rd 8 hours: 25% = 1,980 mls. adult.
BROOKE FORMULA 3. Relieve pain.
Old:  Administer Morphine Sulfate
 0.5 ml/kg B.W./ 1% T.S.B.A. per IV as prescribed. (DOC)
(colloids)  Have Narcan (Naloxone)
 1.5 ml/kg B.W./1% T.S.B.A. readily available (this is the
(crystalloid) 2000 cc of D5W antidote to narcotics if
Revised: (’79): 2-3 ml of respiratory depression occurs)
crystalloids/kg B.W. / 1% T.S.B.A.  Initially, medications are given
EXAMPLE: IV because of sluggish blood
 50% TSBA; 60 kg B.W. flow (increased hematocrit)
60 x 1.5 x 50 = during the first 48 hours post-
4,500 cc = Plain LR burns.
2,000 cc = D5W  Use a bed cradle to relieve
6,500 cc = totals fluids pressure from the top sheet and
 60 x 0.5 x 50 = 1,500 colloids to prevent sticking of exudates
 Hypertonic Na+ = 250mEq/L to the top sheet.
 Lactate 150mEq/L  Avoid exposure of affected
 Cl = 100mEq/L areas to draft. Sudden gush
 EVANS FORMULA: of wind causes hypersensitivity
1.5 ml/kg B.W./1% T.S.B.A. of exposed nerve endings.
0.5 ml/kg B.W./ 1% T.S.B.A. (colloids) Close the door of the client's
room.
INTERPROFESSIONAL COLLABORATIVE 4. Preventing infection.
MANAGEMENT FOR THE PATIENTS  Practice Asepsis. Handwashing
WITH BURNS is the most important practice
include the following: to prevent the spread of
1. Promote respiratory microorganisms.
function.  Implement reverse or
 Assess for sooty sputum and protective isolation.
singed hair in the nose and  Administer Tetanus
eyebrows. (Singed hair is stiff immunization. There is a high
and rigid burnt hair). risk of tetanus infection in
 Establish an open airway. burns. If a history of tetanus
 Administer oxygen therapy. immunization cannot be
2. Promote fluid-electrolyte obtained, or the patient has not
and acid-base balance. received a booster dose for the
 Assess the following last five years, administer
parameters: Immune Globulin.
 Vital signs  Irrigate the affected area with a
 Urine output normal saline (NS) solution.
 Central Venous Pressure 5. Maintain adequate
(CVP) nutrition.
 Level of Consciousness  Do not give oral fluids for
 Weight the first 48 hours. To prevent
 Percentage of Burns paralytic ileus, gastric dilatation
 The vital changes in and water intoxication. SNS
dehydration are as follows: stimulation causes decreased
weight loss, decreased urine gastric motility that results in
output, decreased CVP, and gastric dilatation; and causes
decreased level of decreased peristalsis that
consciousness. Changes in vital results in paralytic ileus.
signs are as follows: elevated Increased ADH secretion causes
body temperature, increased water retention.
pulse rate, rapid respiratory  Provide a high-calorie, high-
rate, and low blood pressure carbohydrate, high-protein
(due to decreased plasma diet. High-calorie, high-
volume). carbohydrate diet provides
 an adequate source of energy. (usually manifested by
A high-protein diet promotes hyperventilation).
healing and tissue repair.  Other side effects may
 Provide a diet rich in include rash, bone
Vitamins A, B and C. Vitamin marrow depression, and
A maintains skin and mucous hemolytic anemia.
membrane integrity. Vitamin B  Silvadene (Silver
enhances metabolism. Vitamin sulfadiazine)
C increases resistance to stress  Apply 1/16-inch film.
and infection.  It does not cause
6. Provide wound care. acidosis.
The different methods of wound  The side effects are as
care are as follows: follows: rash, leukopenia,
 Open method. After and nephritis.
application of the topical  Monitor complete blood
antibiotic, the area is left count (CBC), especially
exposed. This is applicable in the white blood cell
extensive body burns. (WBC) level.
 Semi-open method. The Hydrotherapy
wound is covered with a thin  It is done to remove debris,
layer of sterile gauze after improve circulation, relieve
application of topical antibiotic. pain, promote healing, improve
 Closed method. The wound is muscle tone, and prevent
covered with a thick layer of contractures.
sterile gauze or with occlusive  Administer analgesics 15 to
dressings after the application 30 minutes before
of topical antibiotic. No two hydrotherapy to promote
burn surfaces should be allowed comfort. Immersion into the
to touch; touching can promote water may initially cause pain.
webbing of digits, contractures, Debridement
and poor cosmetic outcomes.  To remove necrotic tissues from
 This is indicated in the burns of the area of burns. It may be
the hands. Apply dressings with surgical or mechanical
the fingers separate from each debridement.
other to prevent contracture  Mechanical debridement is
deformities. Apply a splint on done by wet-to-dry dressings.
the hand with the fingers To do wet-to-dry dressings, do
curbed to allow flexion- the following steps:
extension exercises of the 1. Wash hands.
fingers. This will also prevent 2. Wear clean gloves and remove
nerve damage in the fingers soiled dressing.
and prevent hyperextension 3. Remove gloves and confine
deformity of the fingers. soiled dressing within the
The antimicrobials used in burns are gloves.
as follows: 4. Wear sterile gloves, apply
 Furacin (Nitrofurazone) sterile dressings over the area,
 Apply 1/16-inch film and pour sterile NS solution
directly to the burn area. over the dressing.
 Side effects: rash, 5. Cover the moist dressing with
contact dermatitis. dry dressings (gauze, sponges,
 Sulfamylon (Mafenide or absorbent pads). To maintain
Acetate) the moisture of the wet
 Apply 1/16-inch film dressing.
directly to the burn area. 6. Change the dressing as it
 Administer analgesics becomes dry (or just before) to
before application of the remove the debris. As drying
medication. It causes occurs, wound debris and
local pain. necrotic tissues are absorbed
 The medication may into the gauze dressing by
cause metabolic acidosis capillary action.
(Note: If you are using a sterile  The priority goal of
container with dressings, then pour rehabilitation among burns
sterile NS into the dressings first clients is to prevent or minimize
before dealing with the soiled scarring. The patient may wear
dressings). anti- scar garment for 6
Skin grafting months.
To improve the appearance of  Other goals are to prevent
the affected area. contractures, promote activity
 Isograft or syngeneic graft. The tolerance, and improve body
donor site comes from an image and self-concept.
identical twin. RENAL DISORDERS
 Autograft. The donor site comes THE RENAL SYSTEM, which consists
from the self. of the kidneys, ureters, bladder, and
 Homograft or allograft. The urethra, has two major functions:
donor site comes from another 1. removal of the end products of
human being. metabolism, toxic substances,
 Heterograft or xenograft. The and drugs from the blood and
donor site comes from an then the body, and
animal, e.g., a pigskin. This is 2. regulation of fluid, electrolyte,
temporary. and acid-base balances. These
Care of the Graft Site two functions are accomplished
 Elevate and immobilize the through the formation and
graft site. elimination of urine.
 Keep the site free from ANATOMY AND PHYSIOLOGY
pressure. KIDNEYS:
 Avoid weight bearing.  The two bean-shaped kidneys
 Cleanse the graft from exudates are located retroperitoneally
to prevent infection and (behind the Peritoneum) and
prevent graft adherence. lateral to the thoracic lumbar
 Monitor the graft site for signs area.
and symptoms of infection like  Each kidney is surrounded by a
foul-smelling drainage, fever, thin, fibrous capsule (Bowman’s
elevated WBC, hematoma, or capsule).
edema in the area.
 Instruct the patient on the
following:
 Lubricate healing skin
with cocoa butter lotion.
 Protect the affected area
from sunlight.
 Use splints and support
garments as prescribed.
7. Promote G.I. support. To
prevent stress ulcers
(Curling's ulcer).  Inside the capsule the kidney is
 Insert NGT as indicated. divided into three parts:
 Administer antacids,  the cortex,
and histamine receptor blockers  the medulla, and the
as prescribed.  renal pelvis.
8. Fluid Replacement. To  Blood is supplied to each kidney
prevent hypovolemic shock. through the renal artery, which
Types of fluid replacement enters the kidney at the hilus.
 Colloids: blood, plasma The kidneys receive
expanders (e.g. Hetastarch) approximately through the
 Electrolytes: Lactated Ringers renal cardiac output. Blood
(LR) leaves each kidney through the
 Non-electrolytes: Dextrose 5% renal vein.
in water (D5W)

9. Rehabilitation
 reabsorbed from the tubules
into the capillaries through the
processes of diffusion, osmosis,
and active transport.
SECRETION:
 Certain substances (potassium,
creatinine, and hydrogen) are
actively transported from the
blood into the tubules. Urine
that is formed in the nephrons
consists of nonessential
materials and secretions
 The nephrons, the functional (water, phosphates, and
units of the kidneys, are the sulfates.
sites of urine production.  For every 125 ml. of
 Each kidney contains more than ultrafiltrate, approximately 1
one million nephrons. ml. is excreted as urine.
 Each nephron is composed of a  The remaining 124 ml. is
glomerulus (a network of reabsorbed. Fluids and
capillaries) and a tubular electrolyte balance in the body
system (which consists of is maintained by a negative
the proximal tubule, loop of feedback system between the
Henle, and distal tubule). nephrons and the body’s fluids
and tissues.
 The diluting and concentrating
mechanisms of the nephrons
that regulate the body’s fluid
volumes are controlled
primarily by two hormones:
o Antidiuretic hormone
(ADH), which is produced
by the pituitary gland
and is involved in water
reabsorption,
and aldosterone, which is
produced by the adrenal
 Urine is formed in the nephrons cortex and is involved in
by a combination of three sodium reabsorption and
processes: filtration, potassium secretion.
reabsorption, and secretion.  In addition, the kidney is
FILTRATION: involved in the regulation of the
 Filtration refers to the passage body’s acid-base balance and
of blood through the filtering several metabolic and
membrane of the glomerulus as endocrine functions, e.g.,
a result of pressure differential. secretion of erythropoietin
 The fluid that passes through (which stimulates RBC
the membrane consists of production by the bone
water, electrolytes, and other marrow), metabolism of vitamin
small molecules and is referred D, and secretion of renin (which
to as the ultrafiltrate. as a result of its effect on
 The rate of glomerular filtration angiotensin, is involved in the
is referred to as the glomerular regulation of blood pressure).
filtration rate (GFR); the normal URETERS:
GFR for an average-sized adult  The ureters are the tubes that
male is 125 ml. Per minute. transport urine from the renal
REABSORPTION: pelvis of the kidneys to the
 Essential materials (e.g., bladder. Transport of urine is
glucose, and description, amino accomplished through
acids, Sodium, water) are peristaltic action.
 intercourse, history of recent
UTI, infection with HIV
PATHOPHYSIOLOGY:
 Bacteria ascend to the kidney
and kidney pelvis by way of the
bladder and urethra
 E. coli (85%), K. pneumoniae,
P. mirabilis, Strep. Fecalis, P
aeruginosa, S. aureus

BLADDER:
 The bladder is made of
muscular elastic tissue. It acts
as a temporary reservoir for
urine until it is excreted from
the body. Two muscles control
the opening of the bladder into
the urethra:
 The internal sphincter is
under automatic
(involuntary) nervous
system control.
 The external sphincter is
under central (voluntary)
nervous system control. Inflammation (kidneys grossly
The normal capacity of enlarge)
an adult is 300-500 ml.

PYELONEPHRITIS
 Inflammation of renal pelvis
and parenchyma (functional
kidney tissue)
 Acute pyelonephritis
 Results from an infection
that ascends to
the kidney from CLINICAL MANIFESTATIONS:
the lower urinary tract  Rapid onset with chills and
RISK FACTORS: fever
1. Inability to empty the bladder,  Malaise
Pregnancy  Vomiting
2. Urinary tract obstruction and  Flank pain
congenital malformation  Costovertebral tenderness
3. Urinary tract trauma, scarring  Urinary frequency with burning
4. Renal calculi sensation(dysuria) (bladder
5. Polycystic or hypertensive renal infection)
disease MANIFESTATIONS IN OLDER ADULTS:
6. Chronic diseases, i.e. diabetes  Change in behavior
mellitus  Acute confusion
7. Vesicourethral reflux  Incontinence
8. Instrumentation of the urethra  General deterioration in
& bladder (catheterization, condition
cystoscopy, urologic surgery)
9. Women with increased sexual CHRONIC PYELONEPHRITIS
activity, failure to void after  Involves chronic inflammation
 and scarring of tubules and iodine, seafood,
interstitial tissues of the kidney and radiologic contrast
 Common cause of chronic renal medium, hold testing,
failure and notify physician or
 May develop from chronic radiologist
hypertension, vascular  Voiding cystourethrography:
conditions, severe instill contrast medium into
vesicoureteral reflux, the bladder and use x-ray to
obstruction of urinary tract assess bladder and urethra
 Behaviors when filled and during voiding
1. Asymptomatic  Cystoscopy
2. Mild behaviors: urinary  Direct visualization of
frequency, dysuria, flank pain urethra and bladder
COLLABORATIVE CARE: through cystoscope
 Eliminate causative agent  Used for diagnostic,
 Preventing relapses tissue biopsy,
 Correct contributing factors and interventions
DIAGNOSTIC TESTS:  The client receives local
 Urinalysis: assess pyuria, or general anesthesia
bacteria, and blood cells in
the urine; Bacterial count
 100,000 /ml indicative of
infection Prevent relapse
 Rapid tests for bacteria in urine
 Nitrite dipstick (turning
pink = presence of
bacteria)
 Leukocyte esterase test
(identifies WBC in urine) Diagnostic Tests for adults who have
 Gram stain of urine: identify by recurrent infections or persistent
shape and characteristic (gram bacteriuria
positive or negative); obtain by  Manual pelvic or prostate
clean catch urine or examinations to assess
catheterization structural changes of
 Urine culture and sensitivity: the genitourinary tract, such as
identify infecting organism and prostatic enlargement,
most effective antibiotic; cystocele, rectocele
culture requires 24 – 72 hours
for results; obtain by clean
catch urine or catheterization
 WBC with differential:
leukocytosis and increased
number of neutrophils
 Diagnostic Tests for adults who
have recurrent infections or
persistent bacteriuria
 Intravenous pyelography (IVP)
or excretory urography
 Evaluates structure and
excretory function of
kidneys, ureters, bladder
 Kidneys clear an
MEDICAL MANAGEMENT:
intravenously injected
 Relieving fever & pain
contrast medium that
 Antimicrobial drugs
outlines kidneys, ureters,
 Trimethoprim-
bladder, and
sulfamethoxazole (TMP-
vesicoureteral reflux
SMZ, Septra)
 Intravenous pyelography (IVP)
 Gentamicin w/ or w/out
or excretory urography
ampicillin,
 Check for allergies to
  Cephalosporin
 Ciprofloxacin
 Antispasmodics &
anticholinergics
 relax smooth muscles of
the ureters & bladder,
promote comfort &
increase bladder capacity
 Oxybutynin (Ditropan)
 propantheline (Pro-
Banthine)
NURSING MANAGEMENT:
CLINICAL MANIFESTATIONS:
 Obtain complete medical, drug
 50% are asymptomatic
& allergy histories
 Sudden onset with pronounced
 Assess VS (T°, BP)
symptoms
 Physical exam
 fever, nausea, malaise,
 determine the location of
headache, generalized edema,
discomfort & any signs of
periorbital edema, puffiness
fluid retention (peripheral
around the eyes
edema, shortness of
 Pain or tenderness over the
breath)
kidney area
 Observe & document the
 Mild to moderate hypertension
characteristics of the client’s
 Poor appetite, irritability,
urine
shortness of breath
 Encourage liberal fluid intake if
 Hematuria, convulsions (due to
not contraindicated (3-4L)
hypertension), CHF, oliguria
 Administer prescribed
(UO 100-400ml/day), anuria
medications
(<100 ml/24hr)
 Evaluate laboratory test results
MEDICAL MANAGEMENT:
 BUN, Creatinine, serum
No specific treatment exists guided by
electrolytes, urine culture
the symptoms & the underlying
to determine client
abnormality.
response to therapy
 Bed rest
 Provide health teaching:
 Na+ - restricted diet (edema,
 Provide information
HPN)
about the disease
 Diuretics, antihypertensive
 Medications
drugs
 Increase fluid intake
 Antimicrobials (penicillin)
 Acid-forming diet (meat,
No specific treatment exists guided by
fish, poultry, eggs, corn,
the symptoms & the underlying
cranberries, prunes) – to
abnormality.
prevent Ca++ & MgPO4
 Vitamins to improve general
stone formation
resistance
 Oral iron supplements (anemia)
GLOMERULONEPHRITIS
 Corticosteroids &
 Occurs most frequently in
immunosuppressive agents
children (boys 6-7y/o) & young
adults
 Most clients recover NURSING MANAGEMENT:
spontaneously or with minimal  Monitor VS (BP q4°), and collect
therapy without sequelae daily urine specimens to
 Some develop chronic evaluate client response to
glomerulonephritis treatment
 Most believe that the  Maintain bed rest especially if
inflammatory response is from BP & edema are present
Antigen-Antibody stimulation in  Ensure adequate fluid intake &
the glomerular capillary measure I&O
membrane  Diet: Na & CHON restricted;
adequate CHO intake (prevents
catabolism of body CHON
 stores) emptying of urine)
 Provide health teaching CLINICAL MANIFESTATIONS:
NEPHROTIC SYNDROME  Sudden, sharp, severe flank
 A condition of increased PAIN that travels to the
glomerular permeability that suprapubic region & external
allows larger molecules to pass genitalia (Renal colic, painful
through the membrane into the spasm)
urine and be removed from the  Severity of pain causes nausea,
blood vomiting, and shock.
 Most common cause: Immune  Chills, fever, hypotension (if
or inflammatory process infection develops)
TREATMENT (depends on the cause):  Urinary retention, dysuria
 Immunologic – steroids (obstruction)
 ACE inhibitors – decrease DIAGNOSTIC FINDINGS:
proteinuria  Urinalysis
 Cholesterol-lowering drugs  Gross or microscopic
 Heparin – lower proteinuria & hematuria
renal insufficiency  pH conducive to stone
 GFR is normal – complete CHON formation
diet  ↑SG, mineral crystals,
 GFR is decreased – low CHON casts
diet  ↑Leukocyte (infection)
 Mild diuretics & Na restriction –
edema & HPN
 Assess hydration: vascular
dehydration

UROLITHIASIS
Presence of calculus/calculi (stone) in
the urinary tract
 Nephrolithiasis (kidney)
Urinary casts.
 Ureterolithiasis (ureter)
(A) Hyaline cast (200 X)
(B) Erythrocyte cast (100 X)
(C) Leukocyte cast (100 X)
(D)Granular cast (100 X)

 Radiography (KUB)
RISK FACTORS:  Intravenous Pyelogram (IVP)
 Calciuria, hyperparathyroidism,
calcium-based antacids,
excessive vit. D intake
 Dehydration
 UTI esp. caused by P. mirabilis
(makes urine alkaline & Ca++
ppt.)
 Obstructive d/o (enlarged
prostate)
 Gout (UA crystallizes)
 Osteoporosis
 Prolonged immobility (sluggish
 in renal function
 Reversible with early,
aggressive treatment
CAUSES:
 Prerenal
o Hypovolemic shock
o Cardiogenic shock 2° to
CHF
o Septic shock
o Anaphylaxis
o Dehydration
o Renal artery thrombosis
or stenosis
o Cardiac arrest
 Ultrasonography
Small calculi o Lethal dysrhythmias
 Passed naturally with no  Intrarenal
specific interventions o Ischemia
 Pain is tolerable if the stone is o Nephrotoxicity 2° to
5mm or less in diameter and drugs (aminoglycosides)
moving o Acute & Chronic
 Vigorous hydration glomerulonephritis
 Analgesics (opioids and NSAIDs) o Polycystic disease
 Antimicrobials o Untreated pre & post
Larger calculi renal disorders
 ESWL (extracorporeal shock  Postrenal
wave lithotripsy) o Ureteral calculi
 Laser lithotripsy o Prostatic hypertrophy
SURGICAL MANAGEMENT: o Ureteral stricture
Indicated for large or complicated by o Ureteral or bladder tumor
an obstruction, ongoing UTI, kidney FOUR PHASES OF ARF:
damage, or constant bleeding  Initiation phase
 Percutaneous nephrolithotomy o Begins with the onset of
 Ureterolithotomy the contributing event
 Pyelolithotomy o Reduced blood flow 
NURSING PROCESS: ATN (acute tubular
 Assessment: necrosis)
 History  Death of cells in the
 Pain intensity & location, collecting tubules
Nausea & Vomiting  Oliguric phase
 Vital signs o Begins within 48 hours
 Urine (strain) after the initial cellular
 Diagnosis, Planning, insult (10-14 days or
Interventions longer)
3 main goals o FVE develops (edema,
 Improve urinary HPN, cardiopulmonary
output complications)
 Relieving pain o AZOTEMIA (accumulation
 Preventing
of urea & nitrogenous
infection
waste in the blood) 
neurologic changes,
RENAL FAILURE
seizures, coma, death
 Inability of the nephrons in the
o Low urine SG,
kidneys to maintain Fluid &
hyperkalemia, metabolic
Electrolytes, Acid-Base balance,
acidosis, UREMIA
excrete nitrogen waste products
develops
& perform regulatory function
 Diuretic phase
2 TYPES:
o Diuresis begins as the
ACUTE RENAL FAILURE
nephrons recover
 Sudden, rapid decrease
 o ↑ water content of urine important consideration
but excretion of wastes &  Risk for dehydration-
electrolytes continues to adequately hydrate the client
be impaired  Treat shock & hypotension as
o ↑ BUN, creatinine, K, quickly as possible
phosphate (replacement of fluids & blood)
 Recovery phase  Treat infection promptly
 Continuous renal function
CHRONIC RENAL FAILURE monitoring
 Progressive (months to  Dopamine (Intropin),
years) & irreversible hemodialysis, peritoneal
damage to the nephrons dialysis
 Kidneys are extensively  Diet; low CHON, high calories,
damaged low Na, low K
THREE STAGES OF CRF:  Kayexalate, IV infusion of
 Reduced renal reserve insulin & glucose for
 40 to 75% loss of hyperkalemia
nephron function  Na bicarbonate for acid-base
 Renal insufficiency imbalance
 75 to 90%
 Kidney loses ability to Medical management of CRF is similar
concentrate urine to that for ARF, except the period of
(polyuria, nocturia), treatment is lifelong (unless a kidney
anemia develops transplantation is performed)
 ESRD (End-stage renal disease) Chronic anemia
 <10% of nephrons are Epoetin alfa (Epogen) is administered
functional rather than blood transfusion
 Regular courses of NURSING MANAGEMENT:
dialysis are needed or  Imbalanced nutrition: risk for
kidney transplantation less than body requirements r/t
ASSESSMENT FINDINGS FOR CRF: anorexia
 Elevated BP, weight gain, UO o Monitor & record client’s
decreased dietary intake
 Puffy facial appearance o Provide frequent small
 Pale skin feedings
 GIT ulceration & bleeding o Encourage the client to
 Vague symptoms (lethargy, be involved with food
headache, anorexia, dry mouth) choices & times for
 Pruritus, dry, scaly skin meals
 Urine breath odor, muscle o Explains restrictions &
cramps, bone pain or provide list of nutritional
tenderness & spontaneous needs & acceptable food
fractures can develop choices
  Mental processes (confusion,
depression, seizures, coma)
DIAGNOSTIC FINDINGS :
  BUN, creatinine, K, Mg,
Phosphorus
  RBC count, Hct/Hgb, pH, SG
 IVP – reveals renal dysfunction
 Percutaneous renal biopsy
shows destruction of nephrons
 Radiography & ultrasonography
demonstrate structural defects
in the KUB
 Renal angiography identifies
obstructions in blood vessels
MEDICAL MANAGEMENT:
 Prevention of ARF is an
  BUN elevated (if severe
vomiting and dehydration)
NURSING INTERVENTIONS:
 Maintain NPO until the client
can tolerate oral, intake
 administer medications as
ordered and monitor
effects/side effects
 Notify the physician if
the vomiting pattern changes
 Maintain F & E balance
 Administer, IV fluids as
ordered, keep
an accurate record of l&O
 Record
the amount/frequency of
vomitus
 Assess skin tone/turgor
for degree of hydration
 Monitor
laboratory/electrolyte
values
 Test NG tube drainage or
vomitus for blood,
NAUSEA & VOMITING and bile; monitor pH
Nausea:  Provide measures for maximum
 a feeling of discomfort in the comfort
epigastrium with a conscious  Institute frequent mouth care
desire to vomit; occurs in with tepid water/saline
association with & prior to mouthwashes
vomiting  Remove encrustations around
Vomiting: nares
 forceful ejection of stomach  Keep the head of the bed
contents from the upper GI elevated and avoid sudden
tract (Emetic center in changes in position
the medulla is stimulated (e.g.,  Eliminate noxious stimuli from
by local irritation of intestine or the environment
stomach or disturbance of  Keep the emesis basin clean
equilibrium), causing the  Maintain a quiet environment
vomiting reflex) and avoid unnecessary
CONTRIBUTING FACTORS: procedures
 GI disease  When vomiting subsides:
 CNS disorders (meningitis, CNS  provide clear fluids
lesions) (ginger ale, warm tea) in
 Circulatory problems (CHF) small amounts
 Metabolic disorders (uremia)  gradually introduce solid
 Side effects of certain drugs foods (toast, crackers),
(chemotherapy, antibiotics)  and progress to bland
 Pain foods (baked potato), in
 Psychic trauma small amounts
 Response to motion  Provide client teaching and D/C
ASSESSMENT FINDINGS: planning concerning
 Weakness, fatigue, pallor,  Avoidance of situations, foods,
possible lethargy or liquids that precipitate
 Dry mucous membrane and nausea and vomiting
poor skin turgor/ mobility (if  Need for planned, uninterrupted
prolonged with dehydration) rest periods
 Serum sodium, calcium,  Medication regimen, including
potassium decreased side effects
 Signs of dehydration
  Need for daily weights with after each stool
frequent anthropometric  Need to report worsening
measurement of symptoms
DIARRHEA (abdominal cramps,
 Increase in peristaltic motility, frequency & amount of
producing watery or loosely stool)
formed stools  Need to assess daily
 Diarrhea is a symptom of other weights with frequent
pathological processes anthropometric
CAUSES: measurements
 Chronic bowel disorders,
Malabsorption problems BASIC CONCEPTS IN
 Intestinal infections, Biliary COMMUNICABLE DISEASE AND
tract disorders CHAIN OF INFECTION
 Hyperthyroidism, Saline Communicable Disease Nursing
laxatives The study of an illness due to a
 Magnesium-based antacids specific:
 Stress, Antibiotics, Neoplasms  Toxic substance
 Highly seasoned foods  Occupational exposure
ASSESSMENT FINDINGS:  Infectious agent that affects a
 Abdominal cramps/distension, susceptible individual, either
foul-smelling watery stools, Directly or Indirectly from an:
increased peristalsis  infected animal or person
 Anorexia, thirst, tenesmus,  indirectly through an
anxiety intermediate host,
 Decreased potassium and  vector
sodium if severe  the environment
NURSING INTERVENTIONS: SIGNIFICANT DATA:
 Administer antidiarrheals  signs and symptoms.
 diphenoxylate with  causative agent.
atropine (Lomotil),  mode of transmission.
paregoric, loperamide  diagnostics.
(Imodium),  nursing and medical
and Kaopectate as management through the
ordered; monitor effects. utilization of the nursing
 Control fluid/food intake. process.
 Avoid milk and milk Communicable Disease Concepts
products A Communicable Disease is an illness
 Provide liquids with due to a specific infectious agent or its
a gradual introduction of toxic products that arises through
bland, high-protein, high- transmission of that agent directly or
calorie, low-fat, low-bulk indirectly to a well person or its
foods products from an infected:
 Monitor and maintain fluid and ► Person,
electrolyte status; record ► Animal (vector) or
the number, characteristics, ► Inanimate reservoir (e.g. from a
and amount of each stool. food source or contaminated
 Prevent anal excoriation. water) to a susceptible host.
 Cleanse the rectal area ► Disease is any condition in
after each bowel which the normal structure or
movement with soap and function of an organ or the
water and pat dry body is impaired or damaged.
 Apply ointment or Desitin Physical injuries (open wound =
to promote healing portal of entry) or disabilities
 Use local anesthetic as are not classified as disease,
needed but they can cause disease,
 Provide client teaching and such as infection by a
discharge planning concerning pathogen. Genetics (as in
 Importance of good cancers (↓immune system =
handwashing techniques
 susceptible host) or  Malaria - Palawan, and
deficiencies) can also play a  Filariasis -Mindanao, Leyte,
role in the development of a Bohol & Sorsogon
disease. ► Epidemic disease (seasonal)
► Signs and Symptoms of a is the occurrence of
Disease an unusually large number of
The Signs of disease are objective cases in a relatively short
and measurable (BP, Temp, RR, PR) period.
and can be directly observed by a
clinician or a healthcare worker, while
Symptoms of the disease are
subjective. Symptoms are felt or
experienced by the patient, but they
cannot be clinically confirmed or
objectively measured. This includes
nausea, pain, and fainting sensations.

TWO TYPES OF COMMUNICABLE

DISEASES:
1. Contagious disease is spread
by direct contact with infectious
agents causing the disease and
easily transmitted from one
person to another through
direct or indirect means.
Ex. Measles. Chickenpox
2. Infectious disease is a
disease not only by ordinary
contact but requires direct
inoculation of organisms
through a break in the skin or
mucous membrane.
Ex. AIDS
All communicable diseases are
infectious but not all infectious are
communicable, not all communicable
diseases are contagious, but all
contagious diseases are
communicable.

CLASSIFICATION OF DISEASES BASED

ON OCCURRENCE:
► Sporadic disease is the
intermittent occurrence of a few
isolated unrelated cases in
a given locality; disease occurs
occasionally or irregularly,
with no specific pattern, and
examples are cancers and
degenerative diseases.
► Endemic disease that
continuously occurs throughout
a period, of the usual number of
cases in a given locality,
constantly present in
the population, community, or
country
Examples:
 Different types of pneumonia,
 Schistosomiasis - Samar,
Examples: therapy.
 Dengue fever, July – mid Examples:
 Leptospirosis, Nov.  chicken pox- shingles zoster or
 Mumps, (Rainy
March- herpes zoster.
 Chickenpox, and
 Measles.
April INFECTION
► Pandemic disease(Summer)is an invasion of the body tissue by
epidemic disease that occurs microorganisms and their proliferation
worldwide, the simultaneous (↑numbers).
occurrence of an epidemic of FOUR TYPES OF INFECTION:
the same disease in several 1. Recurrent infection is the
countries. reappearance of symptoms
Examples: after the infectious disease has
 HIV-AIDS, been treated or subsided and
 MERS-COV, the renewed presence of
 SARS and the same infectious agent.
 COVID 19. 2. Re-infection which after an
The Republic Act No. 11332, initial infectious agent has been
repealing Act 3573, otherwise known eliminated, a new infection
as the "Law on Reporting of occurs caused by the same
Communicable Diseases", hereby organism or by another strain
declared the policy of the State to of the same species.
protect and promote the right to 3. Super-infection happens
health of the people and instill health during the period of the illness,
consciousness among them. and additional infection occurs
by another infectious agent.
CLASSIFICATION OF DISEASES BASED Ex. Hepatitis B (pre-requisite) →
ON SEVERITY OR DURATION: Hepatitis D
► Acute disease which develops 4. Autoinfection in which the
rapidly (rapid onset) but lasts infected person is his direct
only a short time and source of re-exposure. The
Examples: infection of a primary host with
 Measles, a parasite, particularly
 Mumps, and Helminthes, in such a way that
 Influenza the complete life cycle of the
► Chronic disease which parasite happens in a single
develops more slowly but lasts organism, without the
for a long period. involvement of another host.
Examples: INFECTIOUS PROCESS (Stages of
 TB and Infection):
 Leprosy. 1. Incubation period extends
from the entry of
► Sub-acute disease which is microorganisms into the body
intermediate between acute to the onset of nonspecific
and chronic, develops rapidly signs and symptoms (fever,
and has long duration. vomiting.
Example: 2. Prodromal period extends
 bacterial endocarditis. from the onset of nonspecific
► Latent disease with signs and symptoms to the
a causative agent remains appearance of specific signs
inactive for a time but then and symptoms which are the
becomes active to produce cardinal or the pathognomonic
symptoms of the disease, an signs.
infection held in check by the 3. Illness period (Acute Phase) in
defensive forces of the body which the host experiences
but activated when the body the maximum impact of
resistance is reduced. the infectious process and
↓Immune System -elderly, specific signs and symptoms
HIV+, radiation therapy, develop and become evident.
stressed, immuno-suppressive 4. Convalescent period is a
 recovery period as  Each link in the chain must be
manifestations subside and favorable to the organism to
signs and symptoms start to cause a disease. Breaking any
abate until the client returns to link can disrupt its
a normal state of health. multiplication, thereby
interrupting the occurrence of
Standard Precautions infection.
The Centers for Disease Control ► The Infectious Agents are
and Prevention (CDC) recommends microbes capable of producing
that blood and body fluid precautions disease. The number of
should be used in all patients. The organisms affects their ability
health care worker should strictly to cause disease, as well as the
implement. (Always wear gloves) susceptibility of the host. For
 Barrier precautions - correct the organisms to cause a
use of PPE or universal barriers disease they must be able to:
 Precautions for invasive  Adhere to the skin and the
procedures mucous membranes.
 Workplace precautions -  Penetrate the skin or mucous
prevent needle injuries; dispose membranes; and
of needles, syringes, and other  Multiply and invade the body's
sharps in puncture-proof natural defenses.
containers.  Bacteria are simple, one-called
TRANSMISSION-BASED PRECAUTIONS: microbes, and some have
1. Airborne precautions require a double-cell membrane that
special handling and ventilation protects them from harm.
procedures to prevent the  Shape (cocci, bacilli,
spread of infection. The use of spirillae)
respiratory protection is  Need for O2(aerobic,
mandatory. (n95 mask) anaerobic)
2. Droplet precautions are  Response to staining
observed because large particle (Gram (+) or (-), acid
droplets do not remain in the fast)
air and generally travel short  Motility (motile, non-
distances, around three feet or motile)
less. (1 meter away  Tendency to capsulate
3. Contact precautions require (encapsulated,
the use of gloves, masks, and capsulated)
gowns. Thorough handwashing  Capacity to form spores
is recommended after (spore-forming, non-
the removal of protective items. spore-forming)
o Spirochetes (Treponema,
THE CHAIN OF INFECTION Leptospira, borrelia)
o Rickettsiae (Rocky Mountain
spotted fever, typhus fever)
o Chlamydiae (urethra, bladder,
fallopian tube and prostate
glands)
 Viruses are the smallest known
microbes. They cannot replicate
independently outside the
host's cells; rather, they invade
 Transmission of infection occurs the host's cells and stimulate
when the agent leaves the them to participate in the
reservoir or host through a formation of additional viruses.
portal of exit and is conveyed  Fungi are found almost
by the mode of transmission everywhere on earth. They live
and enters through an in organic matter, and soil, and
appropriate portal of entry to may be harmful and beneficial.
infect the susceptible host. Some species are used for
 making cheese, yogurt, beer, corresponds to the site where
wine, and certain drugs. Fungal the agent is located. Common
infections in humans are called portals of exit or avenues for
mycoses. secretions, excretions, and
 Protozoa are much larger than droplets are the:
bacteria. Protozoa are the  Respiratory tract - nasal and
simplest single-celled oral discharges.
organisms in the animal  Genitourinary tract (GUT) -
kingdom. Parasitic protozoa urethral secretions.
absorb nutrients from the body  Gastrointestinal tract (GIT) -
of the host. vomitus, stools, some anal
 Parasites live on or within secretions.
other organisms; they live at  The skin and mucous
the expense of others. They membrane - skin infections; and
take their nutrients from their  The placenta (in vertical
hosts, which may cause disease transmission).
and malnutrition. Their ► Mode of Transmission is how
presence may also cause the infectious agent passes
irritation and other problems. from the portal of exit from the
► The Reservoir of Infection reservoir to the susceptible
can be a person, animal, plant, host. This is the easiest link to
the soil, or other substances break in the chain of infections.
where an infectious agent lives  Contact transmission is the
and multiplies until it can infect most common mode of
a susceptible host. Reservoirs transmission. This is divided
are classified into three into:
categories. o Direct contact refers to
 Human Reservoir person-to-person transfer
I. Frank cases or very ill of organisms.
individuals o Indirect contact occurs
II. Sub-clinical or ambulatory when the susceptible
III. Carriers person comes in contact
 The incubatory carrier can with a contaminated
transmit the pathogen during object.
the incubation period before a  Droplet spread is contact with
clinical illness. respiratory secretions produced
 A convalescent carrier is a when the infected person
client who is recovering from coughs, sneezes, or talks.
the illness but continues to Microbes carried in droplets can
shed the pathogenic organism. travel up to three feet, or one
 An intermittent carrier is a meter. The organism is not
person who occasionally sheds suspended in the air but settles
the pathogenic organism. on the surface.
 A chronic or sustained carrier  Vehicle transmission refers
perpetually harbors the to the transmission of
infectious organism in his/her pathogens through water, food,
system. and air.
 Animal reservoirs include  Vector-borne transmission
domesticated and wild animals occurs when intermediate
infected by pathogens. carriers, such as fleas, flies,
 Environmental reservoirs and mosquitoes, transfer the
refer to living and non-living microbes to another living
reservoirs that harbor infectious organism.
pathogens outside the bodies of  Vertical transmission is the
animals. These may exist on passage of a disease-causing
land (plants and soil), in water, agent (pathogen) from the
or in the air. mother to her baby during the
► The Portal of Exit is the route period immediately before and
in which the organism leaves after birth. This transmission
the reservoir. It usually
 might occur across the protection, and
placenta, in the breast milk, or antibodies are
through direct contact during or formed in the
after birth. presence of active
Example: HIV can be a vertically infection (disease)
transmitted pathogen. in the body.
► Portal of Entry is the venue  Active artificial
where the organism infiltrates comes from
the susceptible host. The antigens like
infective microbes use the toxoids or vaccines
same avenues when they exit that can be live
from the reservoir. Controlling attenuated or
the portal of entry involves inactivated
maintaining the integrity of the vaccines are
protective tissues of the host. usually
► A Susceptible Host refers to administered to
an individual who has the the person to
potential to contract an stimulate antibody
infection. The human body has production, all
many defenses against the kinds of
entry and multiplication of immunization, and
microorganisms. When the have many years
host's defenses are good, of protection but
infection will not take place. not lifelong.
However, if the host is in a o Passive immunity is
weakened state, the microbes antibodies that are
can cause an infectious produced by another
disease. source, animal or human,
given to the individual
with long-term effectivity
and have immediate
IMMUNOLOGY AND protection.
IMMUNIZATION  Passive natural
Immunology immunity comes
Immunology is a division of Biology from a
concerned with the study of living transplacental
organisms’ exemption from harmful transfer of
agents. antibodies like
Immunity refers to the body’s breastfeeding with
specific protective response to an colostrum's as a
invading foreign agent or organism. yellowish antibody
TWO TYPES OF IMMUNITY: that boosts the
 Natural immunity is innate immune system of
and non-specific. the baby, transfer
Natural immunity comes in two of IgA, and 6
forms: months to 1-year
o Active immunity which protection.
the host produces its  Passive artificial
antibodies in response to immunity coming
natural antigens and from Immune
these antibodies serum (antibody)
are produced by himself from an animal, or
with long-term effectivity. another human is
 Active natural is injected like
an immunity from tetanus Ig, gamma
a recovery of a globulin, antitoxin,
disease (mumps, antiserum
measles, chicken administration
pox), lifetime with 2-3 weeks
of protection.
  Acquired immunity is secretions creating a vaginal pH
adaptive and specific. of 3.5-4.5. This low pH inhibits
Susceptibility is the reverse of the growth of many disease-
immunity and the result of the producing microorganisms.
suppression of factors that produce  The urethra with the urine
immunity. used for flushing and
 Antigens refer to foreign bacteriostatic action keeps
substances which elicit an bacteria from ascending.
immune response.  The WBC (Leukocytes)
 The three functions of participates both in the natural
immune response: and acquired immune response.
 homeostasis, There are two types of WBC:
 defense and  Granulocytes (Granular
 surveillance. leukocytes)
The body has its natural immunity. Granulocytes (Granular leukocytes) as
They provide a non-specific response classified into:
to any foreign invader, regardless of  Neutrophils with
the invader’s composition. The body polymorphonuclear cells (PMN)
has its anatomic and physiological are the first cells to arrive at
defenses: the site of inflammation and
 Intact skin and mucous increase in acute bacterial
membranes are the body’s infection;
first line of defense against  Eosinophils increase during
microorganisms. It has normal allergic and parasitic infections.
secretions (sweat) that make  Basophils are not usually
skin slightly acidic: Acidity affected by infection.
inhibits bacterial growth.  Agranulocytes (without
 Resident bacteria that granules)
prevent other bacteria from Agranulocytes meaning without
multiplying and use up granules and classified into:
available nourishment.  Monocytes (Macrophages) are
 Nasal Passages that moist phagocytic cells engulfing,
mucous membranes and cilia ingesting, and destroying
trap microorganisms, dust, greater numbers and quantities
and foreign materials. of foreign bodies or toxins.
 Lungs that have alveolar  Lymphocytes consisting of B-
macrophages (large cells and T-cells play a major
phagocytes) which are cells role in Humoral and Cell-
that are responsible for mediated immune response
ingesting microorganisms and and increase in chronic
foreign particles. bacterial and viral infections.
 Oral Cavity sheds mucosal The Inflammatory Responses are
epithelium to rid the mouth of the inflammation that is a local and
colonizers. The flow of saliva nonspecific defensive response of
and it’s partially buffering tissues to an injurious or infectious
action help prevent infection. agent. It is an adaptive mechanism
 The eyes that being protected that destroys or dilutes the injurious
from infection by tears which agent, prevents further spread of
continually wash injury, and promotes the repair of
microorganisms away. damaged tissue.
 Gastrointestinal Tract with There are five characteristic signs of
the high acidity of the stomach inflammation:
that normally prevents bacterial 1. Pain (Dolor);
growth. The resident flora of the 2. Swelling (Tumor);
large intestines prevents the 3. Redness (Rubor);
establishment of disease 4. Heat (Calor) and
producing microorganism. 5. Impaired function of the part.
 The vagina when a girl The lymphoid organs that house
reaches puberty, lactobacilli phagocytic cells and lymphocytes:
ferment sugars in the vaginal  The spleen filters the blood of
 bacteria, viruses, and other hepatitis, and measles.
debris; destroys worn-out RBCs; Presidential decree No. 996
and stores lymphocytes. The (September 16, 1976).
thymus produces thymosin; “Providing for compulsory basic
which programs certain immunization for infants and
lymphocytes to carry out their children below eight years of
protective role. age.”
Immunoglobulins are antibodies MANDATES:
that defend against foreign invaders  Republic Act No. 10152
and the type of defense they will be “Mandatory Infants and
using depends on the structure and Children Health
composition of the antigen and Immunization Act of 2011”
immunoglobulin. There are five types Signed by President Benigno
of immunoglobulins. Aquino III on July 26, 2010. The
They are GAMED mandatory includes basic
Immunoglobulin G (IgG) immunization for children under
Immunoglobulin A (IgA) 5 including other types that will
Immunoglobulin M (IgM) be determined by the Secretary
Immunoglobulin E (IgE) of Health.
Immunoglobulin D (IgD)  EPI Routine Schedule of
Immunization:
IMMUNIZATION is the process by  Wednesday – designated
which vaccines are introduced into the immunization day in all parts of
body before the infection sets in. the country.
 It promotes health and protects  Monthly – in a Barangay Health
children from disease-causing Station (BHS)
agents.  Quarterly – in far-flung areas
 Vaccines are the causative
agent of a disease so modified
as to be incapable of producing
the disease yet at the same
time so little changed that it is
able, when introduced into the
body, to elicit the production of
specific antibodies against the
disease.
These are always antigens; therefore,
they always induce active immunity
when administered thereby causing
the recipient’s immune system to
react to the vaccine that produces
antibodies to fight infection and are
most useful in the prevention of
disease.
EXPANDED PROGRAM ON
IMMUNIZATION (EPI)
 Launched in July 1976 by DOH
in cooperation with the World
Health Organization (WHO)
and UNICEF to ensure that
infants/children and mothers
have access to routinely
recommended infant/childhood
vaccines.
 Vaccination among infants and
newborns (0-12 months)
against seven vaccine-
preventable diseases:
tuberculosis, poliomyelitis,
diphtheria, tetanus, pertussis,
 THE EPI VACCINES AND ITS
CHARACTERISTICS

EPI COLD CHAIN and LOGISTICS:

 Cold Chain Manager = Public
Health Nurse
 Temperature monitoring of
vaccines is done at all levels of
health facilities to monitor
vaccine temperature.
 Temperature checking is done
twice a day early in the
morning and the afternoon
before going home.
 Temperature is plotted every
day in a monitoring chart to
monitor breaks in the cold
chain.
 Vaccine can be stored in
Refrigerator:
 Regional – 6 months
 Municipal / City – 3 months
 Main Health Center – 1 month
Transport Box: 5 days
 FEFO (first expiry and first out)
vaccine is practiced to ensure
that all vaccines are utilized
before their expiry date.
FULLY IMMUNIZED CHILD – when a  Proper arrangement of vaccines
child receives 1 dose of BCG, 3 doses and labeling of vaccines' expiry
of OPV, 3 doses of DPT, 3 doses of date is done to identify those
HBV, and 1 dose of Measles before near expired vaccines
reaching 1 year old.  Vaccine Wastage
 Wastage is defined as loss by
TETANUS TOXOID IMMUNIZATION use, decay, erosion, or leakage
SCHEDULE FOR WOMEN or through wastefulness
Contraindications to Immunization:
 Anaphylaxis or severe
hypersensitivity reaction to a
previous dose of vaccine is an
absolute contraindication to
subsequent doses of vaccine
 A person with a known allergy
ADMINISTRATION OF VACCINES to a vaccine component should
not be vaccinated.
 DPT2 or DPT3 is not given to a
 child who has convulsions or
shock within 3 days after DPT1. MEASLES, GERMAN MEASLES,
Vaccines containing the whole CHICKENPOX, & INFLUENZA
cell pertussis component should Measles (Rubeola; Morbilli)
not be given to children with an  Francis Home (1757) a Scottish
evolving neurological disease physician, who first discovered
(uncontrolled epilepsy or measles. Maurice Hilleman first
progressive encephalopathy). discovered the measles vaccine
 Do not give live vaccines like first available in 1963 and then
BCG to individuals who are improved the vaccine in 1968.
immunosuppressed due to Measles is a childhood infection
malignant disease (child with caused by a virus.
AIDS), going therapy with  Measles is an acute, highly
immunosuppressive agents, or contagious exanthematous,
radiation. vaccine-preventable disease
 A child with a sign and usually affecting children which
symptoms of severe is referred to as upper
dehydration respiratory tract infection
 Fever of 38.5 C and above (URTI).
The following are NOT  It is one of the most common
contraindications. Infants with these and most serious of all
conditions SHOULD be immunized: childhood diseases. An infected
 Allergy or asthma (except if person can release the virus
there is a known allergy to a into the air when they cough or
specific component of sneeze. The measles virus can
the vaccine mentioned above) live on Surfaces for several
 Minor respiratory tract infection hours.
 Diarrhea/vomiting RISK FACTORS:
 Temp. below 38.5 C / low-grade  Being unvaccinated.
fever Unvaccinated children are more
 Family history of adverse at risk of acquiring measles.
reaction following immunization  Traveling internationally.
 Family history of Clients, especially children
convulsions/seizures traveling to developing
 Known or suspected HIV countries (where measles are
infection with no signs and more common) are at higher
symptoms of AIDS risk of catching the disease.
 Child being breastfed  Vitamin A deficiency. A child
 Chronic illnesses such as with a vitamin A-deficient diet is
diseases of the heart, lungs, more likely to have severe
kidney, or liver symptoms and complications.
 Stable neurological condition ETIOLOGIC AGENT:
such as cerebral palsy or Measles is caused by a filtrable virus
Down’s that belongs to the genus Morbilivirus
 Syndrome of the family Paramyxoviridae.
 Premature or low birthweight  The measles virus is rapidly
(vaccination should not be inactivated by heat, ultraviolet
postponed) light, and extreme degrees of
 Recent or imminent surgery acidity and alkalinity.
 Malnutrition  Measles can be serious and
 History of jaundice at birth even fatal for small children.
 >> Generally, one should be While death rates have been
immunized unless the child is falling worldwide as more
so sick that he needs to be children receive the measles
hospitalized. vaccine, the disease still kills
 >> Note: If parents strongly more than 100,000 people a
object to an immunization for a year, most under the age of
sick infant, do not give it. Ask five.
the mother to come back when INCUBATION PERIOD:
the child is well.
  The incubation period is 0-12 rashes erupt. When rashes appear,
days (20 days the longest; eight Koplik's spots disappear.
days the shortest) KOPLIK’S SPOTS
 A single attack usually conveys
lifelong immunity.
MODE OF TRANSMISSION:
 The disease spreads through
direct contact with droplets
released by an infected person
through coughing or sneezing.
The droplets may also land on a
surface, where the viruses
remain active and contagious
for several hours.
 Indirect contact can occur STIMSON’S LINE
through articles or fomites
freshly contaminated with
respiratory secretions of
infected patients.
Fomites - a substance other than
food that may harbor, carry, or
transmit a contagion.
SOURCES OF INFECTION:
 The virus is found in the
patient's blood, as well as in
secretions from the eyes, nose,
and throat.
PERIOD OF COMMUNICABILITY:
 Measles usually lasts about
nine to 10 days, counted from
the beginning of the prodromal II. Eruptive stage
symptoms to the fading of the  The rash is usually seen late on
rash. the fourth day.
 The disease is communicable  A maculopapular rash first
four days before and five days appears behind the ears, along
after the appearance of rashes. the hairline, the cheeks, bridge
 Measles is most communicable of the nose, then covers the
during the height of the rash. entire face, the neck, the trunk,
 About 90% of susceptible and down to the lower
people who are exposed to extremities. The rashes in
someone with the virus will be measles erupt cephalocaudally.
infected.  The rash is fully developed by
CLINICAL MANIFESTATIONS: the end of the second day and
I. Pre-eruptive Stage all symptoms are at their peak
 Fever that usually goes on and during this time.
off  The rash is fully developed by
 catarrhal symptoms manifested the end of the second day and
by rhinitis, conjunctivitis, all symptoms are at their peak
photophobia, and coryza during this time.
 Respiratory symptoms start  High-grade fever that comes on
from common colds to and off.
persistent coughing.  Anorexia and irritability.
 Appearance of enanthem sign  Abdominal tympanism, pruritus,
(Koplik's spot, Stimson's line) lethargy.
 Pathognomonic sign: Koplik's  The throat is red and often
spots extremely sore.
These are inflammatory lesions  As the fever subsides, coughing
of the buccal mucous glands. may diminish, but it often
Koplik's spots usually appear hangs on for a week or two and
one to two days before the measles becomes loose and less
 metallic.  Bronchopneumonia,
III. Stage of convalescence pneumonia, and/or bronchitis
 Rashes fade away in the are common
manner they erupt  Otitis media
 Fever subsides as the eruption  Nephritis
disappears. When the rash  Encephalitis; encephalomyelitis
fades, desquamation begins.  Blindness (seldom)
 Symptoms subside, and the  If a woman is pregnant, there is
appetite returns. a need to take special care to
CLINICAL MANIFESTATIONS: avoid measles because the
The infection occurs in sequential disease can cause preterm
stages over two to three weeks. labor, low birth weight, and
1. Infection and incubation. For the maternal death.
first 10 to 14 days after infection, the TREATMENT MODALITIES:
measles virus incubates. There are no  Anti-viral drugs (Isoprinosine as
signs or symptoms of measles during the drug of choice)
this time.  Antibiotics if the patient is
2. Nonspecific signs and symptoms. present with complications
Measles typically begins with a mild to  Supportive therapy (oxygen
moderate fever, often accompanied inhalation, IV fluids)
by a persistent (metallic/brassy) PREVENTION:
cough, runny nose, conjunctivitis, and If someone in the household has
sore throat. These mild symptoms measles, take note of these
may last two or three days. precautions to protect vulnerable
3. Acute illness and rash. The rash family members and other people.
consists of small red spots, some of 1. Isolation. Measles is highly
which are slightly raised. Spots and contagious from about four days
bumps in tight clusters give the skin a before to five days after the rash
splotchy red appearance. The face breaks out. Patients should minimize
breaks out with rashes first. or avoid interaction with other people
4. Over the next few days, the rash during this period.
spreads down the arms and trunk, It may also be necessary to keep
then over the thighs, legs, and feet. At nonimmunized people, like siblings,
the same time, the fever rises sharply, away from the infected person.
often as high as 40 °C to 41 °C. The 2. Immunization
measles rash gradually recedes,  Anti-measles vaccine is given at
fading first from the face and last from the age of nine months as
the thighs and feet. a single dose unless there is an
outbreak of measles.
UNFAVORABLE SIGNS OF MEASLES:  Mumps, measles, and rubella
 Violent onset with high-grade (MMR) to be given at ages 12
fever to 15 months old, and the
 Fading eruption with rising second dose is given at six to
fever eight years.
 Appearance of hemorrhagic or NURSING MANAGEMENT:
black measles  Isolation (quiet, well-ventilated,
 Persistence of fever for 10 days subdued light in the patient's
or more room)
 Slight eruptions are  Control high temperature with
accompanied by severe warm or tepid sponge baths.
symptoms, especially those of  The patient should have a daily
encephalitis. cleansing bed bath. The water
DIAGNOSTIC PROCEDURES: should be comfortably warm.
 Nose and throat swab  Oral and nasal hygiene are very
 Routine urinalysis important aspects of nursing
 Blood exams (CBC results either care in patients with measles.
with leukopenia or leukocytosis)  The patient is sensitive to light;
 Complement fixation or adjust the position of the
hemagglutinin test patient to avoid direct glares.
COMPLICATIONS: Keep the eyes free of
 secretions. the rash is at its peak. Infants
 Careful attention should be with congenital rubella are
given to the ears. It is the highly communicable cases and
responsibility of the nurse to be may shed the virus a few
on the alert for any signs of months after birth.
early mastoid infection. CLINICAL MANIFESTATIONS:
 Daily elimination is important. I. Prodromal period
This can be accomplished by  Low-grade fever
using a mild laxative or as  Headache, malaise, and mild
prescribed by the physician. coryza, with conjunctivitis
 During the febrile stage, limit  Post-auricular, sub-occipital,
the diet to fruit juices, milk, and and posterior cervical
water. lymphadenopathy which occurs
 If the patient is vomiting, give on the third to the fifth day
iced juices in small amounts after onset
frequently.  Arthralgia, and slight swelling of
 The patient's position should be the joints
changed every three to four II. Eruptive period
hours.  A pinkish rash on the soft
 Penicillin or other prescribed palate (Forchheimer's spot)
medications are usually given in  An exanthematous rash
cases with complications. appears; first on the face, then
spreading to the neck, the
Rubella (German Measles; Three-day arms, trunk, and legs.
Measles)  The eruption appears after the
 Rubella is an acute viral onset of adenopathy.
infection caused by the rubella  Children usually present less or
virus. It causes mild feverish no constitutional symptoms.
illnesses associated with a rash,  The rash may last for one to
joint pains, and swollen lymph five days and leaves no
nodes. It has a teratogenic pigmentation or desquamation.
effect on a fetus, especially  Testicular pain is present in
during the first three months of young adults.
pregnancy.  Transient polyarthralgia and
ETIOLOGIC AGENT: polyarthritis may occur in
 Rubella virus is a togavirus and adults and occasionally in
is closely related to children.
alphaviruses. RISK OF CONGENITAL MALFORMATION:
INCUBATION PERIOD:  100%-when maternal infection
 The duration from exposure to occurs on the first trimester of
the appearance of the rash is pregnancy or first month
usually 14-21 days of gestation
MODE OF TRANSMISSION:  4%-in the second and third
 Direct contact with trimester
nasopharyngeal secretions of  90%- of congenital rubella
infected people. cases will excrete the virus at
 Air droplets. birth and are therefore
 Transplacental in congenital infectious.
rubella.  10% remain contagious until
 Infants with congenital rubella one year of age.
shed large quantities of the (Congenital Rubella)
virus in their pharyngeal Classic congenital rubella syndrome is
secretions and urine, which characterized by:
serve as a source of infection to  the possibility of spontaneous
other contacts. abortion
PERIOD OF COMMUNICABILITY:  cleft palate, harelip, talipes, and
 The disease is communicable eruption of teeth
approximately one week before  intrauterine growth retardation:
and four days after the onset of the infant has a low birth
rashes but is at its worst when weight
  thrombocytopenic purpura reactions in some people. One
known as "blueberry muffin" should not be vaccinated if:
skin o one has a weak immune
 lethargy and hypothermia system due to another
COMPLICATIONS: illness; and
 Encephalitis o if the individual is
 Neuritis, arthritis, arthralgias pregnant or plans to
 Rubella syndrome, manifested become pregnant within
by: the next month.
o Microcephaly congruent NURSING MANAGEMENT:
with mental retardation  Isolation (airborne), with good
o Apart from myocarditis, ventilation
cardiac malformations  Bed rest until the fever
such as patent ductus subsides
arteriosus,  Darken the room to avoid
interventricular septal photophobia.
defect, or pulmonic  Provide a mild but nourishing
stenosis may occur. diet,
o Eye defects such as  Do not apply heat or cold packs
cataracts, corneal on the ears unless ordered.
clouding, chorioretinitis,  Prevent the spread of infection
and microphthalmia. and the occurrence of
o The baby may be deaf complications.
and mute.
o Hepatosplenomegaly, Chickenpox (Varicella)
interstitial pneumonia  Chickenpox or varicella is an
o Delayed growth with acute and highly contagious
poorly functioning organs disease of viral etiology
PREVENTION: characterized by vesicular
 Administer live attenuated eruptions on the skin and
measles, mumps, and rubella mucous membranes with mild
(MMR) vaccine. These are constitutional symptoms.
usually given to children who ETIOLOGIC AGENT:
are between 12 and 15 months  Varicella-zoster (V-Z) virus-a
old (see National Immunization DNA-containing virus.
Schedule).  Humans are the only source of
 Pregnant women should avoid infection.
exposure to patients infected  Closely related or identical to
with rubella. herpes zoster virus
 Administer immune serum INCUBATION PERIOD:
globulin one week after  10 to 21 days may be
exposure to rubella. prolonged after passive
 If one does not know whether immunization against
he/she has been vaccinated for chickenpox.
German measles, it is important MODE OF TRANSMISSION:
to have their immunity tested, 1. Direct contact with patients who
especially if: shed the virus from the vesicles on
o she is a woman of their skin.
childbearing age and is 2. Indirect contact through linens or
not pregnant. fomites.
o working in an educational 3. Airborne, or spread by droplet
or medical facility; or infection
o planning to travel to a PERIOD OF COMMUNICABILITY:
country that does not  Chickenpox is most contagious
offer immunization from one to two days before the
against rubella. rash appears until all the
 While the rubella vaccine is blisters are dried and crusted.
usually not harmful, the virus in The patient is capable of
the shot could cause adverse transmitting the disease about
 a day before the eruption of the vesicle, pustule, and
first lesion up to about five days crust.
after the appearance of the last o Finally, these open
crop. wounds crust over and
CLINICAL MANIFESTATIONS: turn into scabs. As they
 The telltale sign of chickenpox heal, new bumps
is an extremely itchy skin rash continue to appear.
with red blisters. Over several Various kinds of lesions
days, the blisters pop and start may erupt at the same
to leak. Then, they crust and time. The patient can
scab over before healing finally disseminate the virus to
takes place. other people until all the
 Once chickenpox develops, the spots crust over.
varicella-zoster virus stays in DIAGNOSTIC PROCEDURES:
the nerve cells for years. It can  Determination of V-Z virus
"wake up" and become active through complement fixation
again years later. This can lead test
to shingles, a condition that  Determination of V-Z virus
causes painful blisters. through electron microscopic
Fortunately, there is a vaccine examination of vesicular fluid
for shingles, but it is usually COMPLICATIONS:
recommended for adults over  Secondary infection of the
60 years of age. lesions: furuncles, cellulitis, skin
 The signs and symptoms are abscess, and erysipelas
divided into: (bacterial infection,
Pre-eruptive characterized by large, raised
o manifestations red patches on the skin),
characterized by a mild TREATMENT MODALITIES:
fever, malaise, and  Acyclovir (Zovirax) 500
Eruptive stage wherein the mg/tablet, one tab BID for
rash appears. seven days
o The rash starts from the  Oral acyclovir 800 mg TID for
trunk (unexposed area), five days
and then spreads to  Oral antihistamine to
other parts of the body. symptomatic pruritus
o Initial lesions are  Calamine lotion on itchy skin
distinctively red papules  Avoid anti-inflammatory
and contents become painkillers like ibuprofen; it can
milky and pus-like within make the patient feel very ill.
four days. Never give aspirin to children
o In adults and older under 16 years. It can lead to a
children, the lesions are serious complication called
more widespread and Reye's syndrome.
more severe.  Give acetaminophen or
o There is rapid paracetamol for fever and pain
progression so that associated with sores that
the transition is develop on the skin or in the
completed in six to eight buccal cavity. It is safe for most
hours. people, including pregnant
o Vesicular lesions are very women and children over two
pruritic. months old.
o All stages are present PREVENTION:
simultaneously before all  Active immunization with live
are covered with scabs. attenuated varicella vaccine.
All lesions appear in The first shot is given at 12 to 15
different stages at one months of age, and the second is
time, or they will pass administered when the child is four to
through the following six years old. People over age 13 who
stages: macule, papule, have never been vaccinated should
get two doses of the vaccine at least
28 days apart. ETIOLOGIC AGENTS:
 Avoid exposure to infected  RNA-containing myxoviruses,
people as much as possible. types A, A-prime, B, and C
INCUBATION PERIOD:
 The usual incubation period is
NURSING MANAGEMENT: 24-48 hours.
 Respiratory isolation until all MODE OF TRANSMISSION:
vesicles have crusted  Airborne spread in crowded
 Secondary infection of the skin populations
lesion can be prevented  Direct contact through droplet
through hygienic care of the spread
patient.  The influenza virus persists for
 Heat and sweat make the hours in dried mucus.
patient itch more. Use cool, wet PERIOD OF COMMUNICABILITY:
washcloth to soothe very itchy  Until the fifth day of illness; up
areas. to seven days in children
 Nasopharyngeal secretions and CLINICAL MANIFESTATIONS:
discharges should be disposed  The onset is sudden, and the
of properly. Disinfect linens by patient reports a chilly
sunlight or by chemical means. sensation, hyperpyrexia,
 Cut fingernails short and wash malaise, sore throat, coryza,
hands more often to minimize rhinorrhea, myalgia, and
bacterial infections that may be headache.
introduced by scratching.  Severe aches and pain, usually
 Encourage the child to wear at the back, are associated with
mittens. Provide activities to increased sweating.
keep the child occupied to  Sometimes, gastrointestinal
distract him/her from elements (dyspepsia) with
scratching. vomiting are present.
 Clients are advised to see a  The worst symptoms usually
doctor if the following last for three to five days, then
manifestations appear: the patient begins to improve.
a. shortness of breath and  Influenza makes most patients
dizziness. feel terrible, but most people
b. vomiting, stiff neck, and recover.
fever over 38.5 °C. DIAGNOSTIC PROCEDURES:
c. the rash spreads to one or  Viral serology
both eyes; and a. Complement fixation test
d. the rash gets very red, b. Hemo-agglutination test
warm, or tender. This could be a sign c. Neutralization test
of a bacterial skin infection. COMPLICATIONS:
 The major problem posed by
Influenza (La Grippe, Flu) influenza is the subsequent
 Influenza is an acute, highly complications. The most
contagious viral infection of the common one is pneumonia,
respiratory system which is categorized into
characterized by the abrupt primary viral pneumonia,
onset of fever, chills, muscle secondary bacterial pneumonia,
pain, headache, body malaise, and mixed pneumonia (Fauci,
and catarrh. 2008).
 Influenza is a potentially serious  Primary pneumonia is less
disease that can lead to common but more severe. The
hospitalization and sometimes patient fails to defervesce and
even death. Every influenza (or develops progressive dyspnea
"flu") season varies and affects and cough with scanty sputum.
people differently. Millions of Other relevant sequelae are:
people get the flu every year, o encephalitis and other
and hundreds of thousands are neurologic syndromes.
hospitalized and die of flu- o Reye syndrome is an
related causes.
 acute encephalopathy characterized by inflammation
and fatty degeneration of and formation of a false
the liver that is membrane on the throat,
associated with epidemic tonsils pharynx, and larynx that
influenza B infection. hinders breathing and
o myocarditis which may swallowing.
lead to cardiac failure;  Its causative agent produces a
and toxin that causes potentially
o sudden infant death fatal heart and nerve damage.
syndrome (SIDS). Diphtheria can also affect the
 Superimposed bacterial skin and mucous membranes, a
infections due to Streptococcus condition known as wound or
pneumoniae, S. pyogens. cutaneous diphtheria
Haemophilus influenzae and
Staphylococcus aureus may PERTUSSIS (Whooping cough)
occur. The hallmark of • Pertussis is a highly contagious
secondary pneumonia is fever respiratory disease known for
associated with a productive its uncontrollable, violent,
cough. Elderly patients are at repeated spasmodic coughing.
risk of this complication, as well This distinct coughing pattern
as those with cardiac problems. consists of a series of explosive
 Mixed viral and bacterial expirations, typically ending in
pneumonia is the most common a long-drawn forced inspiration
complication of influenza. It has which produces a crowing
clinical features of both viral sound, the "whoop", and is
and bacterial pneumonia. usually followed by vomiting.
MANAGEMENT: MODE OF TRANSMISSION:
Up until recently, there has been no • Pertussis is primarily spread by
specific treatment for influenza, and direct contact and respiratory
the best thing to do is: droplets.
 Stay at home and take plenty of • It may also spread indirectly
rest. through soiled linens and other
 Drink plenty of water. articles contaminated by
 Take the following to relieve respiratory secretions.
fever and headache:
a. Paracetamol
b. aspirin, unless contraindicated
(not to be given to children under the
age of 16) and
c. ibuprofen or other anti-
inflammatory drugs.
 Sponge the patient down with
tepid water.
 Isolate the patient to decrease
the risk of infecting others
(respiratory isolation).
 Limit strenuous activity,
especially in children.
 Watch out for complications.
PREVENTION:
 Immunization
 Avoid crowded places.
 Educate the public about basic
personal hygiene.

DIPTHERIA (Membranous croup)

 Diphtheria is an acute, highly
contagious bacterial disease of
the upper respiratory tract